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KOMA YuichiroGraduate School of Medicine / Faculty of Medical SciencesAssociate Professor
Researcher basic information
■ Research Keyword■ Research Areas
■ Committee History
- Nov. 2022 - Present, 日本消化器癌発生学会, 代議員
- Apr. 2022 - Present, 日本病理学会, 病理専門医研修プログラム審査委員会
- Apr. 2022 - Present, 日本病理学会, 病理専門医制度運営委員会
- Aug. 2021 - Present, 日本がん転移学会, 評議員
- Apr. 2020 - Present, 日本病理学会, 診断病理編集委員会委員
- Oct. 2019 - Present, 日本分子腫瘍マーカー研究会, 世話人
- Apr. 2018 - Present, 日本病理学会, 近畿支部学術委員
- May 2015 - Present, 日本病理学会, 学術評議員
- Apr. 2018 - Apr. 2022, 日本病理学会, 男女共同参画・働き方改革委員会委員
- Jan. 2019 - Dec. 2020, 日本病理学会, Pathology International刊行委員会委員
- Sep. 2019 - Sep. 2020, 日本病理学会, 第38回日本病理学会病理専門医試験実施委員
- 2018 - 2019, 日本消化器癌発生学会, 2018～2019年度理事長直轄プロジェクト特別研究推進・「腫瘍-間質相互作用を標的とした癌進展メカニズムの解明」委員
Research activity information
■ Award- Nov. 2021 日本病理学会, 令和3年度日本病理学会学術研究賞, 間質細胞との細胞間相互作用による腫瘍進展機構の解析
- Aug. 2021 公益財団法人 武田科学振興財団, 2021年度医学系研究助成（がん領域）
- Feb. 2019 日本消化器癌発生学会, 日本消化器癌発生学会 理事長直轄プロジェクト 特別推進研究, 腫瘍ー間質相互作用を標的とした癌進展メカニズムの解明Japan society
- Sep. 2014 日本分子腫瘍マーカー研究会, 日本分子腫瘍マーカー研究会学術奨励賞, マクロファージによるp38 MAP kinaseカスケードの活性化は食道癌の発癌初期段階を促進するJapan society
- Feb. 2009 第90回日本消化器病学会近畿支部例会優秀プレゼンテーション賞
- Oct. 2005 第15回広島がんセミナー優秀ポスター演題賞
- Jun. 2005 第9回日本がん転移学会研究奨励賞
- Tumor-infiltrating macrophages (Mϕs), known as tumor-associated macrophages (TAMs), play a crucial role in the tumor microenvironment. Immunohistochemistry (IHC) revealed that intratumoral CD68-positive Mϕs are associated with poor prognosis and clinicopathological factors in patients with hepatocellular carcinoma (HCC). Subsequently, an indirect co-culture system involving HCC cells and peripheral blood-derived Mϕs was developed. Complementary DNA (cDNA) microarray analysis revealed that C-C motif chemokine ligand 2 (CCL2) was highly expressed in HCC cells co-cultured with Mϕs. CCL2 neutralization suppressed proliferation, migration, and phosphorylation of extracellular signal-regulated kinase (Erk) in HCC cells and Mϕs enhanced through co-culture. In contrast, recombinant human CCL2 (rhCCL2) addition facilitated these malignant phenotypes and increased Erk phosphorylation levels in HCC cells and Mϕs. The primary CCL2 receptor, C-C motif chemokine receptor 2 (CCR2) was expressed in HCC cells and Mϕs and was upregulated in co-cultured HCC cells. CCR2 inhibition suppressed malignant phenotypes and reduced phosphorylated levels of Erk enhanced by rhCCL2. Additionally, the inhibition of Erk signal suppressed rhCCL2-enhanced malignant phenotypes. Moreover, serum CCL2 levels were higher in patients with HCC than those in healthy donors. Based on IHC, CCL2-positive cases with high CCR2 expression and phosphorylated Erk-positive cases exhibited poor survival outcomes. Therefore, CCL2 upregulation through interactions between HCC cells and Mϕs contributed to HCC progression, making the CCL2/CCR2/Erk signal a potential target for HCC treatment.Corresponding, Jan. 2025, The American journal of pathology, English, International magazine[Refereed]Scientific journal
- Cancer-associated fibroblasts (CAFs) are a key component of the tumor microenvironment and significantly contribute to the progression of various cancers, including esophageal squamous cell carcinoma (ESCC). Our previous study established a direct co-culture system of human bone marrow-derived mesenchymal stem cells (progenitors of CAFs) and ESCC cell lines, which facilitates the generation of CAF-like cells and enhances malignancy in ESCC cells. In this study, we further elucidated the mechanism by which CAFs promote ESCC progression using cDNA microarray analysis of monocultured ESCC cells and those co-cultured with CAFs. We observed an increase in the expression and secretion of amphiregulin (AREG) and the expression and phosphorylation of its receptor EGFR in co-cultured ESCC cells. Moreover, AREG treatment of ESCC cells enhanced their survival and migration via the EGFR-Erk/p38 MAPK signaling pathway. Immunohistochemical analysis of human ESCC tissues showed a positive correlation between the intensity of AREG expression at the tumor-invasive front and the expression level of the CAF marker FAP. Bioinformatics analysis confirmed significant upregulation of AREG in ESCC compared with normal tissues. These findings suggest that AREG plays a crucial role in CAF-mediated ESCC progression and could be a novel therapeutic target for ESCC.Corresponding, MDPI AG, Oct. 2024, Cells, 13(20) (20), 1733 - 1733[Refereed]Scientific journal
- (Background) Cancer-associated fibroblasts (CAFs) are major cancer stromal components. CAFs have diverse functions and cell origins. Podoplanin (PDPN), a lymphatic vessel marker, is also a CAF marker in certain cancers. On daily diagnosis of early colorectal carcinoma (CRC), PDPN upregulation in the stroma is often encountered, suggesting PDPN-positive CAFs have emerged. However, PDPN-positive CAFs in early CRC have not been studied well. (Methods) On immunohistochemistry, PDPN expression in the lamina propria or stroma of adenomas, early CRCs, and neuroendocrine tumors, their normal neighbors, and non-neoplastic colorectal lesions were compared. Single-cell RNA sequencing (scRNA-seq) of CRC was used to explore PDPNhigh CAFs’ cell origins. (Results) Reticular cells or pericryptal fibroblasts in the lamina propria of adenomas and early CRCs showed higher PDPN expression than did normal mucosae and non-neoplastic lesions (p < 0.01). Pericryptal PDPN expression was a diagnostic feature of adenomas and early CRCs. scRNA-seq of CRCs highlighted that PDPNhigh CAFs had distinctly higher COL4A1, COL4A2, and WNT5A expression, unlike well-known CAFs characterized by high FAP, POSTN, or ACTA2 expression. (Conclusions) We demonstrated that pericryptal fibroblasts and reticular cells in the lamina propria are origins of early-stage CRC CAFs and thus have potential as a diagnostic marker for distinguishing colorectal non-neoplastic from neoplastic lesions.Last, MDPI AG, Oct. 2024, Cells, 13(20) (20), 1682 - 1682[Refereed]Scientific journal
- Macrophages in the tumor microenvironment, termed tumor-associated macrophages (TAMs), promote the progression of various cancer types. However, many mechanisms related to tumor–stromal interactions in epithelial ovarian cancer (EOC) progression remain unclear. High-grade serous ovarian carcinoma (HGSOC) is the most malignant EOC subtype. Herein, immunohistochemistry was performed on 65 HGSOC tissue samples, revealing that patients with a higher infiltration of CD68+, CD163+, and CD204+ macrophages had a poorer prognosis. We subsequently established an indirect co-culture system between macrophages and EOC cells, including HGSOC cells. The co-cultured macrophages showed increased expression of the TAM markers CD163 and CD204, and the co-cultured EOC cells exhibited enhanced proliferation, migration, and invasion. Cytokine array analysis revealed higher YKL40 secretion in the indirect co-culture system. The addition of YKL40 increased proliferation, migration, and invasion via extracellular signal-regulated kinase (Erk) signaling in EOC cells. The knockdown of integrin β4, one of the YKL40 receptors, suppressed YKL40-induced proliferation, migration, and invasion, as well as Erk phosphorylation in some EOC cells. Database analysis showed that high-level expression of YKL40 and integrin β4 correlated with a poor prognosis in patients with serous ovarian carcinoma. Therefore, the YKL40/integrin β4 axis may play a role in ovarian cancer progression.Corresponding, MDPI AG, Oct. 2024, International Journal of Molecular Sciences, 25(19) (19), 10598 - 10598[Refereed]Scientific journal
- Last, Jun. 2024, Internal medicine (Tokyo, Japan), English, Domestic magazine[Refereed]Scientific journal
- Corresponding, Elsevier BV, Feb. 2024, The American Journal of Pathology[Refereed]Scientific journal
- Abstract Immunohistochemistry is primarily employed to visualize the localization of specific molecules in tissue samples. However, there is an increasing need for software‐assisted quantitative assessment. In the present study, we performed inverted blue channel‐based pseudoimmunofluorescence image analysis using original immunohistochemistry images. In human esophageal squamous cell carcinoma tissues, various humoral factors promote the phosphorylation of signaling proteins, including protein kinase B (Akt) and/or extracellular signal‐regulated kinase 1/2 (ERK1/2), leading to tumor progression. Our method demonstrated applicability in the analysis of localized signaling proteins in histological sections. Relatively high phosphorylated Akt (p‐Akt) intensity was observed in the cancer‐stroma adjacent (Adj) and noncancerous regions of the superficial layer (SL). Furthermore, localized phosphorylated ERK1/2 (Thr202/Tyr204) was observed in the Adj of the SL and invasive front, distinct from the pattern of p‐Akt (Ser473) and p‐Akt (Thr308). In conclusion, pseudoimmunofluorescent immunohistochemistry image analysis is useful for the quantitative assessment and objective interpretation of localized signaling proteins in esophageal squamous cell carcinoma. The method can also be applied to analyze various immunohistochemistry images from diverse tissues.Wiley, Jan. 2024, Pathology International[Refereed]Scientific journal
- Pulmonary tumor thrombotic microangiopathy (PTTM) is a rare and critical malignancy-related disease characterized by acute progressive pulmonary hypertension (PH). In most cases of PTTM, the cancer can be diagnosed in advance. Identification of the primary cancer is valuable for PTTM diagnosis. Here, we present the case of a patient with PTTM due to early gastric carcinoma in whom the diagnosis of malignant cancer was not revealed until macroscopic autopsy findings. This case highlights the importance of recognizing causative occult early gastric cancer leading to PTTM in cases of acute progressive PH.Jan. 2024, Pulmonary circulation, 14(1) (1), e12359, English, International magazine[Refereed]
- Herein, we report a rare case of a carcinoma with primitive phenotype (enteroblastic and/or hepatoid differentiation) occurring at a colostomy site. The patient was an elderly male who underwent neoadjuvant chemoradiotherapy for rectal cancer, followed by abdominoperineal resection. A biopsy specimen for the rectal carcinoma before neoadjuvant chemoradiotherapy was conventional tubular adenocarcinoma. Moreover, a pathological complete response was confirmed in the proctectomy specimen. However, a colostomy-site tumor appeared 6 months after the proctectomy, and it was resected 1 year after the initial proctectomy. The colostomy-site tumor comprised solid to focal glandular growth of atypical polygonal cells with clear to pale eosinophilic cytoplasm and was immunohistochemically positive for cytokeratin, spalt-like transcription factor 4, glypican-3, caudal type homeobox 2, and special AT-rich sequence-binding protein 2. Thus, the tumor was diagnosed as poorly differentiated adenocarcinoma with primitive phenotype, with suggested origin from the colorectal epithelium. Additionally, a multilocular cystic lesion comprising various types of epithelia was found adjacent to the tumor, suggestive of metaplasia or heterotopia. Changes in the histology and immunophenotype, and the findings of an adjacent cystic lesion suggest a metachronous tumor rather than a recurrence of the primary tumor.Dec. 2023, Pathology international, English, International magazine[Refereed]
- Tumor-associated macrophages (TAMs) are abundant in the tumor microenvironment and are considered potential targets for cancer immunotherapy. To examine the antitumor effects of agents targeting human TAMs in vivo, we here established preclinical tumor xenograft models based on immunodeficient mice that express multiple human cytokines and have been reconstituted with a human immune system by transplantation of human CD34+ hematopoietic stem and progenitor cells (HIS-MITRG mice). HIS-MITRG mice supported the growth of both human cell line (Raji)– and patient-derived B cell lymphoma as well as the infiltration of human macrophages into their tumors. We examined the potential antitumor action of an antibody to human SIRPα (SE12C3) that inhibits the interaction of CD47 on tumor cells with SIRPα on human macrophages and thereby promotes Fcγ receptor–mediated phagocytosis of the former cells by the latter. Treatment with the combination of rituximab (antibody to human CD20) and SE12C3 inhibited Raji tumor growth in HIS-MITRG mice to a markedly greater extent than did rituximab monotherapy. This enhanced antitumor effect was dependent on human macrophages and attributable to enhanced rituximab-dependent phagocytosis of lymphoma cells by human macrophages. Treatment with rituximab and SE12C3 also induced reprogramming of human TAMs toward a proinflammatory phenotype. Furthermore, the combination treatment essentially prevented the growth of patient-derived diffuse large B cell lymphoma in HIS-MITRG mice. Our findings thus support the study of HIS-MITRG mice as a model for the preclinical evaluation in vivo of potential therapeutics, such as antibodies to human SIRPα, that target human TAMs.Frontiers Media SA, Dec. 2023, Frontiers in Immunology, 14[Refereed]Scientific journal
- Tumor-associated macrophages (TAMs), one of the major components of the tumor microenvironment, contribute to the progression of esophageal squamous cell carcinoma (ESCC). We previously established a direct co-culture system of human ESCC cells and macrophages and reported the promotion of malignant phenotypes, such as survival, growth, and migration, in ESCC cells. These findings suggested that direct interactions between cancer cells and macrophages contribute to the malignancy of ESCC, but its underlying mechanisms remain unclear. In this study, we compared the expression levels of the interferon-induced genes between mono- and co-cultured ESCC cells using a cDNA microarray and found that interferon-inducible protein 16 (IFI16) was most significantly upregulated in co-cultured ESCC cells. IFI16 knockdown suppressed malignant phenotypes and also decreased the secretion of interleukin-1α (IL-1α) from ESCC cells. Additionally, recombinant IL-1α enhanced malignant phenotypes of ESCC cells through the Erk and NF-κB signaling. Immunohistochemistry revealed that high IFI16 expression in human ESCC tissues tended to be associated with disease-free survival and was significantly associated with tumor depth, lymph node metastasis, and macrophage infiltration. The results of this study reveal that IFI16 is involved in ESCC progression via IL-1α and imply the potential of IFI16 as a novel prognostic factor for ESCC.Corresponding, MDPI AG, Nov. 2023, Cells, 12(22) (22), 2603 - 2603[Refereed]Scientific journal
- Hepatic inflammatory pseudotumors (IPTs) are defined as benign, non-malignant, non-metastasizing tumors characterized by the presence of myofibroblastic spindle cells, hetorogenous populations of inflammatory cells, particularly plasma cells, lymphocytes and macrophages, as well as locations of fibrosis and necrosis without cellular anaplasia or atypical mitoses. Despite subsequent reports in the references, hepatic IPT remains difficult to diagnose; while posing major issues specifically for its differential diagnosis compared with that of other various benign diseases and malignant hepatic tumors. Histopathological findings are always a requisite for confirming the diagnosis, particularly given that the pathogenesis of IPT remains ambiguous to date. Hepatic IPT is a heterogeneous entity in terms of its clinical features, pathological findings, and pathogenesis. Once the diagnosis is confirmed, however, needless surgery such as wedge resection and lobectomy should be avoided. Here, we discuss the heterogeneity of hepatic IPT, its clinical features, pathological findings, and pathogenesis, and describe its differential diagnosis.Sep. 2023, Diagnostics (Basel, Switzerland), 13(17) (17), English, International magazine[Refereed]Scientific journal
- Abstract M2 macrophages contribute to the progression of oesophageal squamous cell carcinoma (ESCC); however, the roles of M2 macrophages in early ESCC remain unclear. To clarify the biological mechanisms underlying the interaction between M2 macrophages and oesophageal epithelial cells in early‐stage ESCC, in vitro co‐culture assays between the immortalised oesophageal epithelial cell line Het‐1A and cytokine‐defined M2 macrophages were established. Co‐culture with M2 macrophages promoted the proliferation and migration of Het‐1A cells via the mTOR–p70S6K signalling pathway activated by YKL‐40, also known as chitinase 3‐like 1, and osteopontin (OPN) that were hypersecreted in the co‐culture supernatants. YKL‐40 and OPN promoted the above phenotypes of Het‐1A by making a complex with integrin β4 (β4). Furthermore, YKL‐40 and OPN promoted M2 polarisation, proliferation, and migration of macrophages. To validate the pathological and clinical significances of in vitro experimental results, immunohistochemistry of human early ESCC tissues obtained by endoscopic submucosal dissection (ESD) was performed, confirming the activation of the YKL‐40/OPN–β4–p70S6K axis in the tumour area. Moreover, epithelial expression of β4 and the number of epithelial and stromal infiltrating YKL‐40‐ and OPN‐positive cells correlated with the Lugol‐voiding lesions (LVLs), a well‐known predictor of the incidence of metachronous ESCC. Furthermore, the combination of high expression of β4 and LVLs or high numbers of epithelial and stromal infiltrating YKL‐40‐ and OPN‐positive immune cells could more clearly detect the incidence of metachronous ESCC than each of the parameters alone. Our results demonstrated that the YKL‐40/OPN–β4–p70S6K axis played important roles in early‐stage ESCC, and the high expression levels of β4 and high numbers of infiltrating YKL‐40‐ and OPN‐positive immune cells could be useful predictive parameters for the incidence of metachronous ESCC after ESD. © 2023 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.Corresponding, Wiley, Jul. 2023, The Journal of Pathology, 261(1) (1), 55 - 70, English[Refereed]Scientific journal
- Tumor-associated macrophages (TAMs) contribute to disease progression in various cancers, including esophageal squamous cell carcinoma (ESCC). We have previously used an indirect co-culture system between ESCC cell lines and macrophages to analyze their interactions. Recently, we established a direct co-culture system to closely simulate actual ESCC cell-TAM contact. We found that matrix metalloproteinase 9 (MMP9) was induced in ESCC cells by direct co-culture with TAMs, not by indirect co-culture. MMP9 was associated with ESCC cell migration and invasion, and its expression was controlled by the Stat3 signaling pathway in vitro. Immunohistochemical analyses revealed that MMP9 expression in cancer cells at the invasive front (“cancer cell MMP9”) was related to high infiltration of CD204 positive M2-like TAMs (p < 0.001) and was associated with worse overall and disease-free survival of patients (p = 0.036 and p = 0.038, respectively). Furthermore, cancer cell MMP9 was an independent prognostic factor for disease-free survival. Notably, MMP9 expression in cancer stroma was not associated with any clinicopathological factors or patient prognoses. Our results suggest that close interaction with TAMs infiltrating in cancer stroma or cancer nests induces MMP9 expression in ESCC cells, equipping them with more malignant features.Corresponding, MDPI AG, May 2023, Cancers, 15(11) (11), 2987 - 2987[Refereed]Scientific journal
- BACKGROUND: A 70-year-old man with hepatitis C virus-related recurrent hepatocellular carcinoma was admitted for further diagnosis of a 1 cm iso-hyperechoic nodule in segment (S) 5. CASE SUMMARY: Gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid-enhanced magnetic resonance imaging (EOB-MRI) revealed the nodule in S5 with a defect at the hepatobiliary phase, hyperintensity on diffusion weighted imaging (DWI) and hypointensity on apparent diffusion coefficient (ADC) map. Contrast-enhanced computed tomography revealed hypervascularity at the early phase, and delayed contrast-enhancement was observed at the late phase. Contrast-enhanced ultrasound (US) revealed incomplete defect at the late vascular phase. Inflammatory liver tumor, lymphoproliferative disease, intrahepatic cholangiocarcinoma (small duct type) and bile duct adenoma were suspected through the imaging studies. US guided biopsy, however, showed a noncaseating hepatic sarcoid-like epithelioid granuloma (HSEG), and histopathological analysis disclosed spindle shaped epithelioid cells harboring Langhans-type multinucleated giant cells. One month after admission, EOB-MRI signaled the disappearance of the defect at the hepatobiliary phase, of hyperintensity on DWI, of hypointensity on ADC map, and no stain at the early phase. CONCLUSION: That the patient had received BNT162b2 messenger RNA (mRNA) coronavirus disease 2019 vaccination 3 mo before the occurrence of HSEG, and that its disappearance was confirmed 4 mo after mRNA vaccination suggested that the drug-induced sarcoidosis-like reaction (DISR) might be induced by the mRNA vaccination. Fortunately, rechallenge of drug-induced DISR with the third mRNA vaccination was not confirmed.Jan. 2023, World journal of clinical cases, 11(1) (1), 177 - 186, English, International magazine[Refereed]
- High infiltration of tumor-associated macrophages (TAMs), which contribute to the progression of several cancer types, is correlated with poor prognosis of esophageal squamous cell carcinoma (ESCC). In addition to the previously reported increase in migration and invasion, ESCC cells co-cultured directly with macrophages exhibited enhanced survival and growth. Furthermore, interleukin-related molecules are associated with ESCC; however, the precise mechanism underlying this association is unclear. Therefore, we explored the role of interleukin-related molecules in ESCC progression. A cDNA microarray analysis of monocultured and co-cultured ESCC cells revealed that the interleukin 7 receptor (IL-7R) was upregulated in ESCC cells co-cultured with macrophages. Overexpression of IL-7R promoted the survival and growth of ESCC cells by activating the Akt and Erk1/2 signaling pathways. The IL-7/IL-7R axis also contributed to the promotion of ESCC cell migration via the Akt and Erk1/2 signaling pathways. Furthermore, immunohistochemistry showed that ESCC patients with high IL-7R expression in cancer nests exhibited a trend toward poor prognosis in terms of disease-free survival, and showed significant correlation with increased numbers of infiltrating macrophages and cancer-associated fibroblasts. Therefore, IL-7R, which is upregulated when directly co-cultured with macrophages, may contribute to ESCC progression by promoting the development of various malignant phenotypes in cancer cells.Corresponding, MDPI AG, Jan. 2023, Cancers, 15(2) (2), 394 - 394, English, International magazine[Refereed]Scientific journal
- Jan. 2023, BIOMEDICINES, 11(1) (1), English[Refereed]Scientific journal
- Wiley, May 2022, Oral Diseases[Refereed]Scientific journal
- Corresponding, Elsevier BV, Dec. 2021, The American Journal of Pathology, 192(3) (3), 536 - 552, English[Refereed]Scientific journal
- Esophageal cancer has the sixth highest mortality rate worldwide. Cancer-associated fibroblasts (CAFs) are involved in the progression of various cancers. Previously, we demonstrated an association between high expression of the CAF marker, fibroblast activation protein, and poor prognosis of esophageal squamous cell carcinoma (ESCC). We also established CAF-like cells by indirect co-culture of bone marrow-derived mesenchymal stem cells with ESCC cell lines and found metallothionein 2A (MT2A) to be highly expressed in them. Here, to explore the function of MT2A in CAFs, we silenced MT2A in the CAF-like cells and ESCC cell lines using small interfering RNA. MT2A knockdown in the CAF-like cells suppressed expression and secretion of insulin-like growth factor binding protein 2 (IGFBP2); recombinant IGFBP2 promoted migration and invasiveness of ESCC cells via NFκB, Akt, and Erk signaling pathways. Furthermore, MT2A knockdown in the ESCC cell lines inhibited their growth, migration, and invasiveness. Immunohistochemistry demonstrated that high MT2A expression in the cancer stroma and cancer nest of ESCC tissues correlated with poor prognosis of ESCC patients. Hence, we report that MT2A in CAFs and cancer cells contributes to ESCC progression. MT2A and IGFBP2 are potential novel therapeutic targets in ESCC.Corresponding, Sep. 2021, Cancers, 13(18) (18), English, International magazine[Refereed]Scientific journal
- Sep. 2021, Clinics in Oncology, 6(1) (1), 1848Limitation of Modified RECIST - Two Hepatocellular Carcinoma Cases Achieving Radiological Response Incompatible with Histopathological Analysis.[Refereed]
- Jul. 2021, Annals of Clinical and Medical Case Reports, V7(2) (2), 1 - 7Iron Deposit Central Large Nodule in Alagille Syndrome[Refereed]
- BACKGROUND: Metastasis occurs as a late event in the natural history of hepatocellular carcinoma (HCC), and most patients die of liver failure attributed to the tumor supplanting the liver. Conversely, the brain is a less common metastatic site. CASE SUMMARY: We describe a rare case of hepatitis C virus-related multiple HCC metastasizing to the cavernous sinus, Meckel's cave, and the petrous bone involving multiple cranial nerves in an 82-year-old woman. At admission imaging studies including Gadolinium-ethoxybenzyl-diethylenetriamine pentaacetic acid-enhanced magnetic resonance imaging (MRI) revealed multiple HCC nodules in both right and left lobes. Ultrasound guided biopsy of the left lobe revealed moderately differentiated HCC. Molecular targeted therapy with Lenvatinib (8 mg/d for 94 d, per os) and Ramucirumab (340 mg/d and 320 mg/d, two times by intravenous injection) were administered for 4 mo, resulting in progression of the disease. Three months after the start of molecular target therapy, the patient presented with symptoms of hyperalgesia of the right face and limited abduction of the right eye, indicating disturbances in the right trigeminal and abducens nerves. Brain MRI disclosed a mass involving the cavernous sinus, Meckel's cave and the petrous bone. Contrast-enhanced MRI with gadolinium-chelated contrast medium revealed a well-defined mass with abnormal enhancement around the right cavernous sinus and the right Meckel's cave. CONCLUSION: The diagnosis of metastatic HCC to the cavernous sinus, Meckel's cave, and the petrous bone was made based on neurological findings and imaging studies including MRI, but not on histological examinations. Further studies may provide insights into various methods for diagnosing HCC metastasizing to the craniospinal area.Jun. 2021, World journal of hepatology, 13(6) (6), 709 - 716, English, International magazine[Refereed]
- BACKGROUND: The mortality of oral squamous cell carcinoma (OSCC) has remained high for decades; therefore, methods for early detection of OSCC are warranted. However, in the oral cavity, various mucosal diseases may be encountered, including reactive lesions and oral potentially malignant disorders, and it is difficult to differentiate OSCC from these lesions based on both clinical and histopathological findings. It is well known that chronic inflammation contributes to oral cancer development. Macrophages are among the most common inflammatory cells in cancer stromal tissue and have various roles in cancer aggressiveness. Although the roles of macrophages in cancer development have attracted attention, only a few studies have linked macrophages to carcinogenesis, particularly, oral precancerous lesions. SUMMARY: This review article consists of 3 parts: first, we summarize current knowledge on macrophages in human various epithelial precancerous lesions, excluding the oral cavity, to show the importance and gaps in knowledge regarding macrophages in carcinogenesis; second, we review published data related to the role of macrophages in oral carcinogenesis; finally, we present a novel view on oral carcinogenesis, focusing on crosstalk between epithelial cells and macrophages. Key Messages: The biological features of macrophages in oral carcinogenesis differ drastically depending on the anatomical compartment that they infiltrate. Focusing on the alteration of macrophage infiltrating compartment may serve as a useful novel approach for studying the role of the macrophages in oral carcinogenesis and for gaining further insight into cancer prevention and early detection.May 2021, Pathobiology : journal of immunopathology, molecular and cellular biology, 88(5) (5), 1 - 11, English, International magazine[Refereed]Scientific journal
- Tumor-associated macrophages (TAMs) promote tumor progression. The number of infiltrating TAMs is associated with poor prognosis in esophageal squamous cell carcinoma (ESCC) patients; however, the mechanism underlying this phenomenon is unclear. cDNA microarray analysis indicates that the expression of chemokine (C-C motif) ligand 1 (CCL1) is up-regulated in peripheral blood monocyte-derived macrophages stimulated using conditioned media from ESCC cells (TAM-like macrophages). Here, we evaluated the role of CCL1 in ESCC progression. CCL1 was overexpressed in TAM-like macrophages, and CCR8, a CCL1 receptor, was expressed on ESCC cell surface. TAM-like macrophages significantly enhanced the motility of ESCC cells, and neutralizing antibodies against CCL1 or CCR8 suppressed this increased motility. Recombinant human CCL1 promoted ESCC cell motility via the Akt/proline-rich Akt substrate of 40 kDa/mammalian target of rapamycin pathway. Phosphatidylinositol 3-kinase or Akt inhibitors, CCR8 silencing, and neutralizing antibody against CCR8 could significantly suppress these effects. The overexpression of CCL1 in stromal cells or CCR8 in ESCC cells was significantly associated with poor overall survival (P = 0.002 or P = 0.009, respectively) and disease-free survival (P = 0.009 or P = 0.047, respectively) in patients with ESCC. These results indicate that the interaction between stromal CCL1 and CCR8 on cancer cells promotes ESCC progression via the Akt/proline-rich Akt substrate of 40 kDa/mammalian target of rapamycin pathway, thereby providing novel therapeutic targets.Corresponding, Elsevier BV, Apr. 2021, The American journal of pathology, 191(4) (4), 686 - 703, English, International magazine[Refereed]Scientific journal
- Cancer-associated fibroblasts (CAFs) contribute to the progression of various cancers. Previously, we reported the significance of CAFs in esophageal squamous cell carcinoma (ESCC); however, the functions of CAFs in the ESCC microenvironment remain unknown. To investigate CAFs' function, we established an indirect coculture assay between human bone marrow-derived mesenchymal stem cells (MSCs) and ESCC cells. Cocultured MSCs expressed more fibroblast activation protein, one of the markers of CAFs, compared with monocultured MSCs. Therefore, we defined cocultured MSCs as CAF-like cells. To identify molecules associated with the ESCC progression in CAFs, we conducted a cDNA microarray analysis on monocultured MSCs and CAF-like cells to compare their gene expression profiles. We found that SERPINE1, which encodes plasminogen activator inhibitor-1 (PAI-1), was more abundant in CAF-like cells than in monocultured MSCs, and the PAI-1 derived from CAF-like cells induced the abilities of migration and invasion in both ESCC cells and macrophages by the Akt and Erk1/2 signaling pathways via the low-density lipoprotein receptor-related protein 1 (LRP1), which is a PAI-1 receptor. Based on immunohistochemistry assays of ESCC tissues, higher expression levels of PAI-1 and LRP1 were correlated with poor prognosis in ESCC patients. These results suggest that the PAI-1/LRP1 axis contributes to the progression of ESCC, making it a potential target for ESCC therapy.Corresponding, Mar. 2021, Laboratory investigation; a journal of technical methods and pathology, 101(3) (3), 353 - 368, English, International magazine[Refereed]Scientific journal
- Background: CD163-positive macrophages contribute to the aggressiveness of oral squamous cell carcinoma. We showed in a previous report that CD163-positive macrophages infiltrated not only to the cancer nest but also to its surrounding epithelium, depending on the presence of stromal invasion in tongue carcinogenesis. However, the role of intraepithelial macrophages in tongue carcinogenesis remains unclear. In this study, we assessed the biological behavior of intraepithelial macrophages on their interaction with cancer cells. Materials and Methods: We established the indirect coculture system (intraepithelial neoplasia model) and direct coculture system (invasive cancer model) of human monocytic leukemia cell line THP-1-derived CD163-positive macrophages with SCC25, a tongue squamous cell carcinoma (TSCC) cell line. Conditioned media (CM) harvested from these systems were analyzed using cytokine array and enzyme-linked immunosorbent assay and extracted a specific upregulated cytokine in CM from the direct coculture system (direct CM). The correlation of both this cytokine and its receptor with various clinicopathological factors were evaluated based on immunohistochemistry using clinical samples from 59 patients with TSCC. Moreover, the effect of this cytokine in direct CM on the phenotypic alterations of THP-1 was confirmed by real-time polymerase chain reaction, western blotting, immunofluorescence, and transwell migration assay. Results: It was shown that CCL20 was induced in the direct CM specifically. Interestingly, CCL20 was produced primarily in SCC25. The expression level of CCR6, which is a sole receptor of CCL20, was higher than the expression level of SCC25. Our immunohistochemical investigation showed that CCL20 and CCR6 expression was associated with lymphatic vessel invasion and the number of CD163-positive macrophages. Recombinant human CCL20 induced the CD163 expression and promoted migration of THP-1. We also confirmed that a neutralizing anti-CCL20 antibody blocked the induction of CD163 expression by direct CM in THP-1. Moreover, ERK1/2 phosphorylation was associated with the CCL20-driven induction of CD163 expression in THP-1. Conclusions: Tongue cancer cell-derived CCL20 that was induced by interaction with macrophages promotes CD163 expression on macrophages.2021, Frontiers in oncology, 11, 667174 - 667174, English, International magazine[Refereed]Scientific journal
- Drug-induced pancreatitis is often mild to moderate in severity, but severe and even fatal cases can occur. Here, we report a 74-year-old woman undergoing chemotherapy for recurrent renal cell carcinoma, who presented with abdominal pain after administration of pazopanib following nivolumab and was diagnosed with severe acute pancreatitis. Administration of methylprednisolone and conservative treatment were initiated, but clinical findings and laboratory tests rapidly worsened. When she died, an autopsy was performed. The autopsy findings suggested the possibility of pancreatitis as immune-related adverse events. To the best of our knowledge, no fatal cases of acute pancreatitis due to nivolumab or pazopanib have been reported. We considered that the effects of nivolumab were sustained in the pancreas, and pazopanib administration might have worsened the toxicity.Nov. 2020, Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 21(1) (1), 21 - 24, English, International magazine[Refereed]Scientific journal
- Tumor-associated macrophages (TAMs) contribute to the progression and mortality of various malignancies. We reported that high numbers of infiltrating TAMs were significantly associated with tumor progression and poor prognosis in esophageal squamous cell carcinoma (ESCC). In our previous investigation of TAMs' actions in ESCC, we compared gene expression profiles between peripheral blood monocyte (PBMo)-derived macrophages and TAM-like macrophages stimulated with conditioned media of ESCC cell lines. Among the upregulated genes in the TAM-like macrophages, we focused on CC chemokine ligand 3 (CCL3), which was reported to contribute to tumor progression in several malignancies. Herein, we observed that not only TAMs but also ESCC cell lines expressed CCL3. A CCL3 receptor, CC chemokine receptor 5 (CCR5) was expressed in the ESCC cell lines. Treating the ESCC cell lines with recombinant human (rh)CCL3 induced the phosphorylations of Akt and ERK, which were suppressed by CCR5 knockdown. Migration and invasion of ESCC cells were promoted by treatment with rhCCL3 and co-culture with TAMs. TAMs/rhCCL3-promoted cell migration and invasion were suppressed by inhibition of the CCL3-CCR5 axis, PI3K/Akt, and MEK/ERK pathways. Treatment with rhCCL3 upregulated MMP2 and VEGFA expressions in ESCC cell lines. Our immunohistochemical analysis of 68 resected ESCC cases showed that high expression of CCL3 and/or CCR5 in ESCC tissues was associated with poor prognosis. High CCR5 expression was associated with deeper invasion, presence of vascular invasion, higher pathological stage, higher numbers of infiltrating CD204+ TAMs, and higher microvascular density. High expression of both CCL3 and CCR5 was an independent prognostic factor for disease-free survival. These results suggest that CCL3 derived from both TAMs and cancer cells contributes to the progression and poor prognosis of ESCC by promoting cell migration and invasion via the binding of CCR5 and the phosphorylations of Akt and ERK. The CCL3-CCR5 axis could become the target of new therapies against ESCC.Corresponding, Springer Science and Business Media LLC, Sep. 2020, Laboratory investigation; a journal of technical methods and pathology, 100(9) (9), 1140 - 1157, English, International magazine[Refereed]Scientific journal
- Oral lichenoid conditions (OLC), including oral lichen planus (OLP), oral lichenoid lesions and oral lichenoid dysplasia, differ in pathogenesis and biological malignancy. However, distinguishing them based on clinical or histological features is difficult. It is well known that CD163+ macrophages are associated with oral cancer aggressiveness. We recently demonstrated that CD163+ macrophages of noncancerous lesions infiltrate the stroma, not the intraepithelial area. In this report, we describe a case of OLC that was not detected as malignant by the first local biopsy. Furthermore, we evaluated the malignant potency of OLC by retrospectively comparing the histological findings between local biopsy and resected specimens focusing on CD163+ macrophages. A 72-year-old man with a white lesion in the unilateral buccal mucosa was diagnosed with OLP through the biopsy although invasive cancer was detected two years later. Intraepithelial CD163+ macrophages were found not only on the resected specimen but also biopsy. This is the first report to demonstrate that intraepithelial CD163+ macrophages may be noteworthy indicators to identify the malignant potency of OLC.MDPI AG, Aug. 2020, Diagnostics (Basel, Switzerland), 10(9) (9), 624 - 624, English, International magazine[Refereed]Scientific journal
- OBJECTIVE: Oral leukoplakia has mixed and differing histopathological features, and it is thus difficult to reach an accurate histological diagnosis of oral leukoplakia based on a local biopsy alone. We recently demonstrated the significance of CD163+ macrophages in oral carcinogenesis. Herein we sought to determine whether CD163+ macrophages in biopsy specimens of oral leukoplakia help identify the overall histological nature of the lesion. PATIENTS AND METHODS: Twenty-six patients with tongue leukoplakia who underwent a histological examination by both a preoperative local biopsy and consecutive total excision were enrolled. We evaluated clinicopathological factors and the expression of CD163+ macrophages based on a retrospective comparison of the histological diagnostic concordance between the biopsies and excisions. RESULTS: Seventeen patients (diagnostic-agreement group) were diagnosed with squamous intraepithelial lesion based on both the biopsy and the excision. Nine patients (diagnostic-discrepancy group) were diagnosed with invasive cancer by excision, although invasive cancer was not observed in their biopsy specimens. Compared to the diagnostic-agreement group, the diagnostic-discrepancy group had more tongue leukoplakia with non-homogenous or high numbers of intraepithelial CD163+ macrophages. CONCLUSION: The evaluation of intraepithelial CD163+ macrophages in local biopsy specimens from tongue leukoplakia patients is a promising tool for cancer screening.Apr. 2020, Oral diseases, 26(3) (3), 527 - 536, English, International magazine[Refereed]Scientific journal
- Oral verruciform xanthoma (OVX) is an uncommon benign lesion that is characterized histologically by the accumulation of several foamy macrophages in the lamina propria papillae. The pathogenesis of OVX has not been completely elucidated, although the significance of macrophage polarization (M1, tumor suppression; and M2, tumor promotion) and the contribution of M2 macrophages to angiogenesis are well established. This study investigated the role of foamy macrophages in OVX, with a focus on angiogenesis. Four patients who underwent surgical excision or total excisional biopsy for OVXs were enrolled in this study. We evaluated the expression of the macrophage markers CD68 (broad) and CD163 (M2) and the CD34-positive microvessel density (MVD) of OVXs. The foamy macrophages of all patients exhibited positivity to CD68 and CD163. We evaluated the MVD and the expression of the vascular endothelial growth factor (VEGF) based on histological architecture. The MVD of all OVX cases was significantly higher than that of the corresponding normal epithelia. Interestingly, the MVD of verrucous-type OVX cases was higher than that of the other type. VEGF was expressed on foamy macrophages in all cases. Overall, the foamy macrophages expressing CD163 were associated with the morphogenesis of OVX through the process of angiogenesis by VEGF expression.Feb. 2020, Dentistry journal, 8(1) (1), English, International magazine[Refereed]Scientific journal
- 2020, Japanese Journal of Gastroenterology and Hepatology.Gastric schwannoma with regional lymphadenopathy diagnosed by endoscopic ultrasonography-guided biopsy.[Refereed]Scientific journal
- OBJECTIVES: Growth differentiation factor 15 (GDF15), which is derived from tumor-associated macrophages (TAM) and cancer cells, promotes progression of esophageal squamous cell carcinomas (ESCC). However, its role in the ESCC microenvironment remains unclear. Here, we examined the effects of GDF15 on ESCC cell lines and tissues. METHODS: Western blotting, MTS, and Transwell migration/invasion assays were used to evaluate cell signaling, proliferation, and migration/invasion, respectively, in ESCC cell lines treated with recombinant human GDF15 (rhGDF15). ESCC cell lines were administered a TGF-βRI/II inhibitor (LY2109761), small interfering RNA against TGF-β type II receptor (TGF-βRII), or neutralizing antibody against TGF-βRII to study the role of TGF-βRII in mediating the effects of rhGDF15. The localization of GDF15 and TGF-βRII in ESCC cell lines was observed by immunofluorescence. TGF-βRII expression in ESCC tissues was analyzed by immunohistochemistry, and the relationship between clinicopathological factors and prognosis in ESCC patients was evaluated. RESULTS: rhGDF15 increased levels of phosphorylated Akt, Erk1/2, and TGF-βRII in ESCC cell lines. Inhibition/knockdown of TGF-βRII suppressed rhGDF15-induced activation of Akt and Erk1/2 and enhancement of cellular proliferation, migration, and invasion. Immunofluorescence revealed that TGF-βRII and GDF15 were colocalized in ESCC cell lines. High TGF-βRII expression in ESCC tissues, as determined by immunohistochemistry, correlated with depth of invasion and increased number of infiltrating TAMs. ESCC patients with high TGF-βRII expression showed a tendency toward poor prognosis. CONCLUSIONS: GDF15 promotes ESCC progression by increasing cellular proliferation, migration, and invasion via TGF-βRII signaling.2020, Pathobiology : journal of immunopathology, molecular and cellular biology, 87(2) (2), 100 - 113, English, International magazine[Refereed]Scientific journal
- Dec. 2019, Ann Case Report.Non-B Non-C related hepatocellular carcinoma with sarcomatous change due to epithelial mesenchymal transition.[Refereed]Scientific journal
- Dec. 2019, Ann Case Report.Multiple HNF-1α inactivated type hepatocellular adenoma due to intrahepatic portosystemic venous shunt.[Refereed]Scientific journal
- Objective: Accumulating evidence suggests that macrophages are involved in the immunoediting of oral squamous cell carcinoma but the role of macrophages in oral carcinogenesis is unclear. We aimed to clarify the role of macrophages in oral leukoplakia, which is the most common oral potentially malignant disorder from immunotolerance viewpoint. Materials and methods: The study included 24 patients who underwent surgical resection for tongue leukoplakia. The relationships between macrophage markers and clinicopathological factors were assessed. Conditioned medium was harvested from the CD163+ human monocytic leukaemia cell line, THP-1. The phenotypic alteration of human oral keratinocytes by the conditioned medium treatment was assessed using quantitative reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. Moreover, the clinical samples were evaluated using immunohistochemistry. Results: Tongue leukoplakia tissues with high CD163+ macrophage infiltration were associated with significantly higher degrees of epithelial dysplasia, abnormal Ki-67 expression and cytokeratin13 loss when compared with the tissues with low CD163+ macrophage infiltration. In vitro, CD163+ THP-1 conditioned medium induced immunosuppressive molecules, especially interleukin-10 (IL-10) in human oral keratinocytes. The IL-10 expression levels showed significant positive correlations with not only the numbers of FOXP3+ regulatory T cells but also that of CD163+ macrophages. Conclusions: In tongue leukoplakia, CD163+ macrophages infiltration correlates with immunosuppressive cytokine IL-10 expression.Dec. 2019, Clinical and experimental dental research, 5(6) (6), 627 - 637, English, International magazine[Refereed]Scientific journal
- Oct. 2019, Ann Case Report.Differential diagnosis of small HCC focusing on pseudolymphoma and bile duct adenoma.[Refereed]Scientific journal
- Interleukin-6 (IL-6) is one of the pleiotropic cytokines and has received attention as a critical factor implicated in the invasion and the angiogenesis of various cancers. In glioma, IL-6 is known to be associated with the prognosis; however, the roles of IL-6 in cerebrospinal fluid (CSF) has not been studied sufficiently. We examined the concentration of CSF IL-6 using 75 CSF samples of glioma (54 glioblastomas (GBMs) and 21 other grades of gliomas) and analyzed the association CSF IL-6 with infiltration levels of tumor-associated macrophages (TAMs) and prognosis. The concentration of CSF IL-6 in GBM patients was significantly higher than that in other grades of gliomas. CSF IL-6 levels were associated with the infiltration rate of TAMs in GBMs, and IL-6 levels were increased in the GBM cells co-cultured with TAM-like macrophages. The CSF of GBM patients, which contained high concentration of IL-6, promoted the migration ability of GBM cells, and neutralization antibodies of IL-6 inhibited its migration ability. Finally, in both univariate and multivariate analysis, higher CSF IL-6 levels were associated with poorer prognosis in GBM patients. These results indicated that the concentration of CSF IL-6 is associated with TAMs' infiltration level and may be a useful prognostic biomarker for the GBM patients.Oct. 2019, Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia, 68, 281 - 289, English, International magazine[Refereed]Scientific journal
- Esophageal squamous cell carcinoma (ESCC) is a highly aggressive tumor with frequent recurrence even after curative resection. The tumor microenvironment, which consists of non-cancer cells, such as cancer-associated fibroblasts (CAFs) and tumor-associated macrophages (TAMs), was recently reported to promote several cancers, including ESCC. However, the role of CAF as a coordinator for tumor progression in ESCC remains to be elucidated. In our immunohistochemical investigation of ESCC tissues, we observed that the intensity of expression of two CAF markers-alpha smooth muscle actin (αSMA) and fibroblast activation protein (FAP)-in the tumor stroma was significantly correlated with the depth of tumor invasion, lymph node metastasis, advanced pathological stage, and poor prognosis. We co-cultured human bone marrow-derived mesenchymal stem cells (MSCs) with ESCC cells and confirmed the induction of FAP expression in the co-cultured MSCs. These FAP-positive MSCs (which we defined as CAF-like cells) promoted the cell growth and migration of ESCC cells and peripheral blood mononuclear cell-derived macrophage-like cells. CAF-like cells induced the M2 polarization of macrophage-like cells. A cytokine array and ELISA revealed that CAF-like cells secreted significantly more CCL2, Interleukin-6, and CXCL8 than MSCs. These cytokines promoted the migration of tumor cells and macrophage-like cells. The silencing of FAP in CAF-like cells attenuated cytokine secretion. We compared cell signaling of MSCs, CAF-like cells, and FAP-silenced CAF-like cells; PTEN/Akt and MEK/Erk signaling were upregulated and their downstream targets, NF-κB and β-catenin, were also activated with FAP expression. Silencing of FAP attenuated these effects. Cytokine secretion from CAF-like cells were attenuated by inhibitors against these signaling pathways. These findings indicate that the collaboration of CAFs with tumor cells and macrophages plays a pivotal role in tumor progression, and that FAP expression is responsible for the tumor promotive and immunosuppressive phenotypes of CAFs.Jun. 2019, Laboratory investigation; a journal of technical methods and pathology, 99(6) (6), 777 - 792, English, International magazine[Refereed]Scientific journal
- May 2019, Pathology international, 69(5) (5), 306 - 308, English, International magazine[Refereed]
- Tumor-associated macrophages (TAMs) have important roles in the growth, angiogenesis and progression of various tumors. Although we have demonstrated the association of an increased number of infiltrating CD204+ TAMs with poor prognosis in esophageal squamous cell carcinomas (ESCCs), the roles of TAMs in ESCC remain unclear. Here, to study the effects of TAMs on the tumor microenvironment of ESCCs, we established a co-culture assay using a human ESCC cell line and TAM-like peripheral blood monocyte-derived macrophages and performed a cDNA microarray analysis between monocultured and co-cultured ESCC cell lines. Our qRT-PCR confirmed that in the co-cultured ESCC cell lines, CYP1A1, DHRS3, ANXA10, KLK6 and CYP1B1 mRNA were highly up-regulated; AMTN and IGFL1 mRNA were down-regulated. We observed that the high expression of a calcium-dependent phospholipid-binding protein ANXA10 was closely associated with the depth of invasion and high numbers of infiltrating CD68+ and CD204+ TAMs and poor disease-free survival (P = 0.0216). We also found ANXA10 promoted the cell growth of ESCC cell lines via the phosphorylation of Akt and Erk1/2 pathways in vitro. These results suggest that ANXA10 induced by the interaction with TAMs in the tumor microenvironment is associated with cell growth and poor prognosis in human ESCC tissues.Mar. 2019, Pathology international, 69(3) (3), 135 - 147, English, International magazine[Refereed]Scientific journal
- We review the significance of cancer-stromal interactions (CSIs) in the development, morphogenesis and progression of human gastric and esophageal cancer based on the data obtained from co-culture experiments. Orthotopic fibroblasts in the gastric cancer stroma not only promoted their growth by cancer cells but were also responsible for the mobility, morphogenesis and epithelial-to-mesenchymal transition (EMT) of the cancer cells through CSI. Bone marrow-derived mesenchymal stem cells could be part of the origin of cancer-associated fibroblasts (CAFs) of the gastric cancer providing an advantageous microenvironment for the restoration of cancer stem cells with the induction of the EMT. Tumor-associated macrophages (TAMs) may differentiate from bone marrow-derived monocytes/macrophages within the tumor microenvironment of esophageal cancer and participate in the growth and the progression of esophageal squamous cell carcinomas (ESCCs). Macrophages infiltrated into the intraepithelial neoplastic lesions of the esophagus may function as a biological promoter by promoting the growth and motility of squamous epithelia. Tumor cells build up "cancer as a tissue" by taking advantage of the existing network of growth factors, cytokines and chemokines through the interactions of TAMs, CAFs and cancer cells themselves.Jun. 2018, Pathology international, 68(6) (6), 334 - 352, English, International magazine[Refereed]Scientific journal
- Tumor-associated macrophages (TAMs) are involved in tumor progression and poor prognosis in several malignancies. We previously demonstrated the interaction between high numbers of infiltrating TAMs and poor prognosis in esophageal squamous cell carcinomas (ESCCs). To investigate the significance of TAMs in ESCC, we conducted a cDNA microarray analysis of peripheral blood monocytes (PBMo)-derived macrophages and PBMo-derived macrophages stimulated with conditioned media of TE-series ESCC cell lines (TAM-like PBMo-derived macrophages). C-X-C motif chemokine ligand 8 (CXCL8) was up-regulated in the TAM-like PBMo-derived macrophages. Here we confirmed a high expression level of CXCL8 in TAM-like PBMo-derived macrophages and the expression of CXCR1/2, known as CXCL8 receptors, in TE-series ESCC cell lines. Recombinant human CXCL8 induced the ESCC cell lines' migration and invasion by the phosphorylation of Akt and Erk1/2. In indirect co-cultures, not only signal pathway inhibitors but also neutralizing antibodies against CXCL8, CXCR1 and CXCR2 suppressed these phenotypes induced by TAM-like PBMo-derived macrophages. Immunohistochemical analysis of 70 resected ESCC samples showed that high expression levels of CXCL8 in ESCC tissues were significantly associated with lymph node metastasis and poor prognosis. These results suggest that CXCL8 up-regulated in the microenvironment may contribute to ESCC progression by promoting cancer cells' migration and invasion.Dec. 2017, Oncotarget, 8(62) (62), 106071 - 106088, English, International magazine[Refereed]Scientific journal
- Feb. 2017, Int Surg, English[Refereed]Scientific journal
- Jan. 2017, World journal of clinical cases, 5(1) (1), 18 - 23, English, International magazine[Refereed]Scientific journal
- Oct. 2016, The Journal of pathology, 240(2) (2), 211 - 23, English, International magazine[Refereed]Scientific journal
- Sep. 2016, Cancer letters, 380(1) (1), 47 - 58, English, International magazine[Refereed]Scientific journal
- Feb. 2016, Pathology international, 66(2) (2), 83 - 93, English, International magazine[Refereed]Scientific journal
- We report a rare case of polypoid leiomyosarcoma of the esophagus that was treated by endoscopic submucosal dissection (ESD). A 63-year-old man with complaints of progressive dysphagia was referred to Hyogo Cancer Center for treatment of esophageal tumor. Esophagoscopy revealed a polypoid tumor 25 mm in diameter on the left side of the upper esophagus. Despite several biopsy specimens, the diagnosis could not be confirmed. Computed tomography showed a protruded, homogeneously enhancing mass in the upper esophagus, but no lymph node enlargement or metastasis. After 1.5 months, the esophagogram showed a filling defect 47 mm in diameter in the upper esophagus. Given this rapid tumor growth, en bloc resection was done by ESD for therapeutic diagnosis. After this treatment, the tumor seemed to grow larger, showing a short stalk and occupying the esophageal lumen. Histopathologically, the tumor comprised pleomorphic spindle cells with mitosis. Tumor invasion involved the lumina propria mucosae and contact with the muscularis mucosae, but not involving the submucosa. Immunohistochemical examination showed positive staining for smooth muscle actin and HHF35, but negative for desmin, caldesmon, CD34, c-kit, DOG1, ALK, S-100 protein and cytokeratin. These histopathological findings were compatible with a diagnosis of esophageal leiomyosarcoma derived from the muscularis mucosae.Sep. 2015, Digestive endoscopy : official journal of the Japan Gastroenterological Endoscopy Society, 27(6) (6), 700 - 3, English, International magazine[Refereed]Scientific journal
- May 2015, Laboratory investigation; a journal of technical methods and pathology, 95(5) (5), 491 - 503, English, International magazine[Refereed]Scientific journal
- Mar. 2015, Cancer medicine, 4(3) (3), 437 - 46, English, International magazine[Refereed]Scientific journal
- Dec. 2014, Oncology letters, 8(6) (6), 2621 - 2623, English, International magazine[Refereed]Scientific journal
- Jun. 2013, ESOPHAGUS, 10(2) (2), 108 - 113, English[Refereed]Scientific journal
- OBJECTIVE: Overexpression of phosphatase of regenerating liver-3 (PRL-3) has been implicated in tumor progression and metastasis of gastric carcinoma. Here we examined what alterations occur in the phenotype of gastric cancer cells in vitro and in vivo when PRL-3 expression is knocked down. METHODS: We constructed a small interfering RNA (siRNA)-expressing vector which stably interfered with PRL-3 expression and was transfected into SH101-P4 cells, which express the highest PRL-3 mRNA levels among 13 gastric cancer cell lines. The new SH101-P4 subclones, in which PRL-3 was stably reduced, were established and their in vitro growth, motility and abilities of liver metastasis from the injected spleen were analyzed in vivo. RESULTS: PRL-3 knockdown effectively suppressed invasion and growth of SH101-P4 cells in vitro. Liver metastasis in vivo was significantly decreased when PRL-3 expression was suppressed. The primary tumor size in the injected spleen tended to be smaller in PRL-3 knockdown clones than in the controls. These findings suggest that PRL-3 expression may contribute not only to the establishment of metastasis but also to the growth of primary foci of human gastric cancer. Therefore, PRL-3 may be one of the target molecules in gastric cancer therapy.2010, Pathobiology : journal of immunopathology, molecular and cellular biology, 77(3) (3), 155 - 62, English, International magazine[Refereed]Scientific journal
- We describe an 8-mm hepatocellular carcinoma (HCC) with hepatitis C virus-related cirrhosis in a 74-year-old woman. Ultrasound (US) revealed an 8-mm hyperechoic nodule in segment 6 of the liver. Contrast-enhanced computed tomography (CT) and US revealed no hypervascularity in the early phase and no washout in the late phase and the Kupffer phase, respectively. CT during arteriography revealed no hypervascularity and CT during arterial portography disclosed no perfusion defect. Gadolinium-ethoxybenzyl-diethylenetriamine pentaacetic acid (Gd-EOB-DTPA)-enhanced magnetic resonance imaging (MRI) revealed no hypervascularity in the early phase, but disclosed a defect in the hepatobiliary phase. Histologically, the nodule was diagnosed as well-differentiated HCC characterized by more than two-fold the cellularity of the non-tumorous area, with a high nuclear:cytoplasmic ratio, increased cytoplasmic eosinophilia, fatty change, and slight cell atypia with an irregular thin trabecular pattern. Our case demonstrates the utility of Gd-EOB-DTPA-enhanced MRI in the diagnosis of small HCC.Jul. 2009, Case reports in gastroenterology, 3(2) (2), 187 - 192, English, International magazine[Refereed]
- Scirrhous hepatocellular carcinoma displaying atypical findings on imaging studies.We describe a 15-mm scirrhous hepatocellular carcinoma (HCC) in a 60-year-old man with B-type cirrhosis. Ultrasound disclosed a 15-mm hypoechoic nodule in segment 7. Contrast-enhanced US revealed heterogeneous, not diffuse, hypervascularity in the early phase and a defect in the Kupffer phase. Contrast-enhanced computed tomography (CT) revealed a heterogeneous hypervascular nodule in the early phase and a low-density area in the late phase. Magnetic resonance imaging (MRI) revealed iso- to hypointensity at T1 and high intensity at T2-weighted sequences. Contrast-enhanced MRI also revealed a heterogeneous hypervascular nodule in the early phase and washout in the late phase. Super-paramagnetic iron oxide-MRI revealed a hyperintense nodule. CT during hepatic arteriography and CT during arterial portography revealed heterogeneous hyperattenuation and a perfusion defect, respectively. Based on these imaging findings the nodule was diagnosed as a mixed well-differentiated and moderately-differentiated HCC. Histologically, the nodule was moderately-differentiated HCC characterized by typical cytological and structural atypia with dense fibrosis. Immunohistochemically, the nodule was positive for heterochromatin protein 1 and alpha-smooth muscle actin, and negative for cytokeratin 19. From the above findings, the nodule was diagnosed as scirrhous HCC. Clinicians engaged in hepatology should exercise caution with suspected scirrhous HCC when imaging studies reveal atypical findings, as shown in our case on the basis of chronic liver disease.May 2009, World journal of gastroenterology, 15(18) (18), 2296 - 9, English, International magazine[Refereed]Scientific journal
- BACKGROUND & AIMS: Cell adhesion molecule 1 (CADM1), mediates nerve-mast cell attachment and communication through homophilic binding. An immunohistochemical screen showed that CADM1 is expressed in pancreatic islets. Here, we determined the cell types expressing CADM1 and examined its role in nerve-islet cell interactions. METHODS: Immunohistochemistry and double-staining immunofluorescence were performed on murine and human pancreases and on islet cell tumors (ICTs). alphaTC6 cells, a murine alpha cell line, were cultured on neurite networks of superior cervical ganglia. Neurite-alphaTC6 cell attachment and communication were examined after nerves were activated specifically by scorpion venom. RESULTS: CADM1 was expressed on the plasma membrane in all 4 major types of islet cells, alpha, beta, D, and pancreatic polypeptide in human beings, but primarily in alpha cells in mice. In cocultures, alphaTC6 cell to neurite attachment was inhibited dose-dependently by an anti-CADM1 function-blocking antibody. In response to scorpion venom-evoked nerve activation, 36% of the alphaTC6 cells mobilized Ca(2+), and introduction of a CADM1-targeting small interfering RNA reduced the fraction of responding cells to 7%. In 21 human ICTs, CADM1 was present in the plasma membrane of 7, and the others were negative for CADM1. Six of the CADM1-expressing tumors were functional hormonally, whereas all but 2 of the CADM1-negative tumors were nonfunctional (P = .0032). CONCLUSIONS: CADM1 is a novel islet cell adhesion molecule mediating nerve-islet cell interactions. The strong correlation between CADM1 expression and hormonally functional phenotypes suggests that CADM1 is involved in hormone secretion from ICTs.Lead, May 2008, Gastroenterology, 134(5) (5), 1544 - 54, English, International magazine[Refereed]Scientific journal
- UNLABELLED: Spermatogenic immunoglobulin superfamily (SgIGSF) is an intercellular adhesion molecule of the nectin-like family. While screening its tissue distribution, we found that it was expressed in fetal liver but not adult liver. In the present study, we examined which cells in developing and regenerating liver express SgIGSF via immunohistochemistry and Western blot analysis. In developing mouse liver, SgIGSF expression was transiently upregulated at perinatal ages and was restricted to the lateral membrane of biliary epithelial cells (BECs). In regenerating rat livers from the 2-acetylaminofluorene/partial hepatectomy model, SgIGSF was detected exclusively in oval cells that aligned in ductal and trabecular patterns by the second week posthepatectomy. In human livers, fetal and newborn bile ducts and cirrhotic bile ductules were clearly positive for SgIGSF, whereas disease-free adult bile ducts were negative. To investigate the role of SgIGSF in bile duct/ductule formation, we used an in vitro model in which rat hepatocyte aggregates embedded in collagen gels containing insulin and epidermal growth factor extend epithelial sheets and processes in the first week and form ductules within a month. The process and ductular cells were continuously positive for SgIGSF and cytokeratin 19, a BEC marker. When the aggregate culture was started in the presence of a function-blocking anti-SgIGSF antibody, the number of epithelial processes per aggregate was reduced by 80%. CONCLUSION: We propose that SgIGSF is a novel and functional BEC adhesion molecule that is expressed for a limited time during active bile duct/ductule formation.Mar. 2007, Hepatology (Baltimore, Md.), 45(3) (3), 684 - 94, English, International magazine[Refereed]Scientific journal
- Increased expression of connexin 26 in the invasive component of lung squamous cell carcinoma: significant correlation with poor prognosis.Reduced expression of connexins (Cxs), gap junction proteins, is frequently reported in malignant cell lines and tumors, whereas recent studies suggested that C x 26, a subtype of Cxs, might help tumor cells acquire malignant phenotypes. To examine this suggestion in the clinical setting, 50 lung squamous cell carcinomas (SCCs) were stained with the anti-C x 26 antibody. No C x 26-specific signals were detectable in 34 tumors (group I; 68%), whereas the remaining 16 were judged positive for C x 26 (group II; 32%). In 14 tumors of group II, C x 26-specific signals were detected not in all SCC cells but in SCC cells facing the tumor stroma or capsule, in which the signals were localized on the plasma membrane. Involved lymph nodes of group-II patients often contained metastatic foci consisting of all C x 26-positive cells. The proportion of C x 26-positive to C x 26-negative SCC cells in the metastatic nodes was larger than that in the corresponding primary tumors. C x 26-positive SCC cells seemed to be more invasive and metastatic than negative ones. Consistently, the 5-year cancer-specific survival rate of group-II patients was significantly lower than that of group-I patients (12.5 vs 38.9%; P=0.0391). Multivariate analysis demonstrated that C x 26 expression (P=0.0448) as well as pathological stage (P=0.0338) and vascular invasion (P=0.0191) were independent, significant prognostic predictors. These results suggest that C x 26 may represent an essential effector for controlling the biological aggressiveness of lung SCC tumor.Mar. 2006, Cancer letters, 234(2) (2), 239 - 48, English, International magazine[Refereed]Scientific journal
- Jun. 2005, Journal of immunology (Baltimore, Md. : 1950), 174(11) (11), 6934 - 42, English, International magazine[Refereed]Scientific journal
- Binding of stem cell factor (SCF) to c-kit receptor tyrosine kinase (KIT) transduces signals essential for mast cell development via several pathways including activation of phosphatidylinositol 3-kinase (PI3-K). When cultured mast cells (CMCs) are cocultured with fibroblasts expressing membrane-bound SCF, CMCs with normal KIT adhere to fibroblasts and proliferate, whereas CMCs lacking cell surface expression of KIT do neither. Spermatogenic immunoglobulin superfamily (SgIGSF) was identified as another molecule that participates in mast cell adhesion to fibroblasts. Since the IC-2 mast cell line expressed neither KIT nor SgIGSF, the effect of ectopic expression of KIT or SgIGSF on the adhesion of IC-2 cells was examined. Three forms of KIT with the normal ectodomain were used: wild-type (KIT-WT) and two mutant types with a phenylalanine substitution at the tyrosine residue 719 (KIT-Y719F) or 821 (KIT-Y821F). KIT-Y719F does not activate PI3-K, whereas KIT-Y821F does. Firstly, KIT or SgIGSF was expressed singly in IC-2 cells. All three forms of KIT increased the adhesion level of IC-2 cells, whereas SgIGSF did not. Secondly, SgIGSF was coexpressed with one of the three forms of KIT. Coexpression of SgIGSF with KIT-WT or KIT-Y821F increased the adhesion level more markedly than was achieved by KIT-WT or KIT-Y821F alone. The effect was abolished by an antibody that blocks SCF-KIT interaction. In contrast, coexpression of SgIGSF with KIT-Y719F did not increase the adhesion level induced by KIT-Y719F alone. In adhesion of mast cells to fibroblasts, KIT appeared to behave as an adhesion molecule and as an activator of other adhesion molecules through phosphorylating PI3-K.Lead, Mar. 2005, Laboratory investigation; a journal of technical methods and pathology, 85(3) (3), 426 - 35, English, International magazine[Refereed]Scientific journal
- Distinct roles for the SgIGSF adhesion molecule and c-kit receptor tyrosine kinase in the interaction between mast cells and the mesentery.Intraperitoneal injection of bone marrow-derived mast cells (BMMCs) has therapeutic efficacy against acute bacterial peritonitis. For this role, BMMCs need to settle down the mesentery from the peritoneal cavity. Interaction between BMMCs and the mesentery was examined by using mast cell deficient WBB6F1(F1)-W/Wv [c-kit receptor tyrosine kinase (KIT) mutant], F1-Sl/Sld [KIT ligand stem cell factor mutant], and F1-tg/tg [a practically microphthalmia transcription factor (MITF)-null mutant] mice. Three parameters were measured: the number of BMMCs: (1) developed in the mesentery 5 weeks after intraperitoneal injection into mast cell deficient mice, (2) adhered to mesenteric mesothelial cells, and (3) transmigrated across the mesenteric mesothelial cell monolayer when coculturing both cells for 3 and 18 h, respectively. After intraperitoneal injection, F1-wild type (+/+) BMMCs developed in the mesentery of F1-W/Wv mice but not in that of F1-Sl/Sld mice, while F1-tg/tg BMMCs did not develop, even in the mesentery of WBB6F1-W/Wv mice. In the coculture, WB-W/W BMMCs normally adhered to but poorly transmigrated across F1-+/+ mesothelial cells, and in accordance, F1-+/+ BMMCs normally adhered to but poorly transmigrated across F1-Sl/Sld mesothelial cells. F1-tg/tg BMMCs showed poor adhesion and transmigration, but both parameters were partially but significantly improved by ectopic expression of spermatogenic immunoglobulin superfamily (SgIGSF), a mast-cell adhesion molecule critically regulated by MITF. Since F1-tg/tg BMMCs expressed reduced levels of KIT, these results suggested that SgIGSF and KIT independently played a significant role in the transmigration. Among three parameters, development of mast cells in the mesentery well correlated with the transmigration. This process seemed important for mast cells to settle down from the peritoneal cavity to the mesentery.Nov. 2004, Biochemical and biophysical research communications, 324(2) (2), 782 - 8, English, International magazine[Refereed]Scientific journal
- A derivative of oleamide potently inhibits the spontaneous metastasis of mouse melanoma BL6 cells.We reported previously that the abnormally augmented expression of connexin 26 (Cx26) is responsible for the enhanced spontaneous metastasis of mouse BL6 melanoma cells, and that the exogenous expression of a dominant negative form of Cx26 inhibits the spontaneous metastasis of BL6. Here we show that daily intraperitoneal (i.p.) injections of oleamide, a sleep-inducing lipid hormone, weakly inhibited the spontaneous metastasis of BL6 cells. To obtain a more effective reagent, 19 oleamide derivatives were chemically synthesized and tested for their ability to inhibit the gap junction-mediated intercellular communications (GJIC) that are formed between HeLa cells by the ectopic expression of Cx26 or Cx43. One of these, denoted metastasis inhibitor-18 (MI-18), inhibited the GJIC formed by Cx26 as well as oleamide but unlike oleamide, which is a non-selective inhibitor of connexin, it did not inhibit the GJIC formed by Cx43. Daily i.p. injections of MI-18 potently blocked the spontaneous metastasis of BL6 cells down to 15% of that in the untreated control mice. MI-18 was safe because even after >7 weeks of daily injections, the survival rate of the mice was 93%. We propose that MI-18 may serve as a novel and clinically important prototype of a potent inhibitor of spontaneous metastasis.Oct. 2004, Carcinogenesis, 25(10) (10), 2015 - 22, English, International magazine[Refereed]Scientific journal
- Number of mast cells in the peritoneal cavity of mice: influence of microphthalmia transcription factor through transcription of newly found mast cell adhesion molecule, spermatogenic immunoglobulin superfamily.The mi (microphthalmia) locus of mice encodes a transcription factor, MITF. B6-tg/tg mice that do not express any MITF have white coats and small eyes. Moreover, the number of mast cells decreased to one-third that of normal control (+/+) mice in the skin of B6-tg/tg mice. No mast cells were detectable in the stomach, mesentery, and peritoneal cavity of B6-tg/tg mice. Cultured mast cells derived from B6-tg/tg mice do not express a mast cell adhesion molecule, spermatogenic immunoglobulin superfamily (SgIGSF). To obtain in vivo evidence for the correlation of nonexpression of SgIGSF with decrease in mast cell number, we used another MITF mutant, B6-mi(vit)/mi(vit) mice that have a mild phenotype, ie, black coat with white patches and eyes of normal size. B6-mi(vit)/mi(vit) mice had a normal number of mast cells in the skin, stomach, and mesentery, but the number of peritoneal mast cells decreased to one-sixth that of +/+ mice. Cultured mast cells and peritoneal mast cells of B6-mi(vit)/mi(vit) mice showed a reduced but apparently detectable level of SgIGSF expression, demonstrating the parallelism between mast cell number and expression level of SgIGSF. The number of peritoneal mast cells appeared to be influenced by MITF through transcription of SgIGSF.Aug. 2004, The American journal of pathology, 165(2) (2), 491 - 9, English, International magazine[Refereed]Scientific journal
- Cloning of a soluble isoform of the SgIGSF adhesion molecule that binds the extracellular domain of the membrane-bound isoform.SgIGSF (spermatogenic immunoglobulin superfamily) is a recently identified intercellular adhesion molecule of the immunoglobulin superfamily. In a mast-cell cDNA library, we found a clone that resulted from the retention of intron 7 within the mature SgIGSF message. This clone was predicted to encode a soluble isoform of SgIGSF (sSgIGSF) with 336 amino-acid residues because its open reading frame ended just before the transmembrane domain. We constructed a plasmid expressing sSgIGSF fused to the human IgG Fc fragment at its C-terminus (sSgIGSF-Fc), and transfected it into COS-7 cells. The fusion protein was readily detectable in the culture supernatant. Solid-phase binding assay showed that sSgIGSF interacted directly the extracellular domain of membrane-bound SgIGSF (mSgIGSF). We next examined whether this interaction inhibited homophilic binding of mSgIGSF by aggregation assays using L cells that did not express mSgIGSF. A stable L-cell clone that overexpressed mSgIGSF aggregated with each other but not with mock-transfected L cells, indicating that a homophilic interaction of mSgIGSF mediated the aggregation. Addition of sSgIGSF-Fc inhibited the aggregation of L cells overexpressing mSgIGSF in a dose-dependent manner. Moreover, FACScan analyses revealed the specific binding of sSgIGSF-Fc to mSgIGSF expressed in L cells. Binding of sSgIGSF-Fc to mSgIGSF appeared to inhibit homophilic interactions of mSgIGSF.Lead, Jul. 2004, Oncogene, 23(33) (33), 5687 - 92, English, International magazine[Refereed]Scientific journal
- Contribution of the SgIGSF adhesion molecule to survival of cultured mast cells in vivo.Spermatogenic immunoglobulin superfamily (SgIGSF) is a recently identified adhesion molecule, and the microphthalmia transcription factor (MITF) was essential for its expression in mast cells. Since the tg mutant allele is practically a null mutation of the MITF gene, cultured mast cells (CMCs) derived from (WBxC57BL/6)F(1) (F(1))-tg/tg mice did not express SgIGSF whereas CMCs from F(1)-wild-type (+/+) mice expressed it abundantly. When cocultured with NIH/3T3 fibroblasts, F(1)-tg/tg CMCs showed poor adhesion to NIH/3T3 fibroblasts. When injected intraperitoneally, F(1)-tg/tg CMCs showed poor survival in the peritoneal cavity of mast cell-deficient F(1)-W/Wv mice. SgIGSF was expressed in tg/tg CMCs ectopically through retroviral transfection and through expression of a transgene. The resulting tg/tg CMCs showed not only a better adhesion to NIH/3T3 fibroblasts but also a better survival in the peritoneal cavity than control F(1)-tg/tg CMCs. SgIGSF-mediated adhesion seemed to play a role in the survival of CMCs in the peritoneal cavity.Jun. 2004, Biochemical and biophysical research communications, 319(1) (1), 200 - 6, English, International magazine[Refereed]Scientific journal
- F10, a subline of the B16 mouse melanoma cell line, is itself the parent of the more metastatic BL6 line. BL6 cells differ from F10 cells by an alteration of the gene encoding the B56gamma regulatory subunit of protein phosphatase 2A (PP2A), which results in mRNA encoding a truncated variant of the subunit (deltagamma1). Expression of deltagamma 1 protein is detectable only when BL6 cells are transplanted into mice and then gamma-irradiated. Recently, B56gamma subunit-containing PP2A holoenzymes have shown to dephosphorylate Mdm2, a negative regulator of p53. Thus, we assessed whether the expression of deltagamma1 affects irradiation-induced phosphorylation of Mdm2 and radioresistance of melanoma cells by perturbing the regulation of p53. Western blot analyses revealed that irradiated COS-7 and NIH3T3 cells stably expressing deltagamma1 showed significantly less irradiation-induced Mdm2 phosphorylation. Mdm2 phosphorylation reduces the ability of Mdm2 to target p53 for degradation, which probably explained why p53 protein levels in NIH3T3 cells expressing deltagamma1 were not significantly elevated by irradiation, unlike in wild-type cells. This was also true for F10 cells transfected with deltagamma1 (F10deltagamma1) when the cells expressed deltagamma1 after being irradiated in vivo. p53 mRNA levels in irradiated wild-type and deltagamma 1-expressing cells were both only slightly elevated, suggesting that Mdm2 regulates p53 levels by a post-transcriptional mechanism. p53-mediated induction of the pro-apoptotic gene encoding Bax was also significantly lower in F10deltagamma1 cells irradiated in vivo. Moreover, F10deltagamma1 and BL6 cells were less apoptotic than F10 cells when the cells were irradiated in vivo. The p53 in F10 cells appears to be as functional as that in NIH3T3 cells because irradiation-induced expression of p53-target genes was comparable in both cells. Collectively, deltagamma1 appears to reduce irradiation-induced Mdm2 phosphorylation, which then blocks irradiation-stimulated p53 accumulation. Defects, such as deltagamma1, in PP2A may thus contribute to melanoma cell radioresistance.Lead, Apr. 2004, Histology and histopathology, 19(2) (2), 391 - 400, English, International magazine[Refereed]Scientific journal
- The BL6 subline was derived from the F10 line, which was derived from the B16 mouse melanoma cell line. BL6 cells are more invasive than F10 cells and differ genetically from F10 cells by an alteration of the gene encoding the B56gamma regulatory subunit of protein phosphatase 2A (PP2A). This alteration results in the transcription of mRNA encoding a truncated variant of the B56gamma1 isoform (Delta-gamma-1). Delta-gamma-1 is capable of targeting PP2A to the specific subcellular sites but incapable of promoting the dephosphorylation of specific substrates that is normally mediated by the B56gamma subunit-containing PP2A holoenzyme. It thus appears that activities of this type of holoenzymes decrease in cells expressing Delta-gamma-1. Recently, we found two possible ways how Delta-gamma-1 contributes to the enhanced metastatic potential of BL6 cells. The two ways seemed far away from each other: Delta-gamma-1 influenced both the nuclear and cytoplasmic functions of the cell. In the cytoplasm, Delta-gamma-1 localized at the Golgi complex and accelerated Golgi-mediated vesicle transport. On the other hand, Delta-gamma-1 disturbed the cell-cycle regulation. In response to gamma-irradiation, protein levels of Delta-gamma-1 were markedly increased in BL6 cells. Subsequently the integrity of cell-cycle checkpoint became more aberrant in BL6 cells than that in F10 cells. These two actions of Delta-gamma-1 could results in the enhancement of the malignant phenotypes of melanoma cells, as discussed in this review.Oct. 2003, Histology and histopathology, 18(4) (4), 1313 - 9, English, International magazine[Refereed]Scientific journal
- Members of the immunoglobulin superfamily often play key roles in intercellular adhesion. IGSF4 is a novel immunoglobulin (Ig)-like intercellular adhesion molecule. Three Ig-like domains are included in the extracellular domain of IGSF4 and mediate homophilic or heterophilic interactions independently of Ca2+. The cytoplasmic domain of IGSF4 contains the binding motifs that connect to actin fibers. Since IGSF4 has been characterized by several independent research groups, this molecule is called by three names, TSLC1, SgIGSF and SynCAM. IGSF4 was first characterized as a tumor suppressor of non-small cell lung cancer and termed TSLC1, although how IGSF4 suppresses tumor growth remains unknown. Silencing of the IGSF4 gene was primarily achieved by allelic loss and promoter methylation in this type of cancers. Soon after this discovery, IGSF4 was found to have roles in adhesion of spermatogenic cells to Sertoli cells and mast cells to fibroblasts and termed SgIGSF. Other researchers revealed that IGSF4 drives synaptic formation of neural cells and termed it SynCAM.Oct. 2003, Histology and histopathology, 18(4) (4), 1321 - 9, English, International magazine[Refereed]Scientific journal
- Clinical implication and prognostic significance of the tumor suppressor TSLC1 gene detected in adenocarcinoma of the lung.BACKGROUND: Recently, the TSLC1 (tumor suppressor in lung cancer 1) gene has been identified as a novel tumor suppressor in human nonsmall cell lung carcinoma. To the authors' knowledge, the clinical relevance of TSLC1 gene expression has not been studied using patient data and surgical samples. The current study was designed to evaluate whether the TSLC1 gene can serve as a target for the prognostic determination of patients with pulmonary adenocarcinoma. METHODS: A total of 38 patients who were surgically treated for proven primary lung adenocarcinoma were enrolled in the current study. Surgical specimens were examined for TSLC1 protein expression immunohistochemically and by Western blot analysis. The correlation between levels of TSLC1 expression and pathologic characteristics, as well as prognosis, was investigated. RESULTS: All patients underwent a potentially curative resection of their tumor. TSLC1 antigen expression as evaluated by immunohistochemistry was confirmed by immunoblotting. The expression of TSLC1 protein was found to be inversely correlated with advanced disease stage, lymph node involvement, lymphatic permeation, and vascular invasion. The 4-year overall survival rates of patients with a tumor demonstrating high (> 70% positive cells [n = 14 patients]), intermediate (20-70% positive cells [n = 10 patients]), and low (< 20% positive cells [n = 14 patients]) expression of the TSLC1 antigen were 84%, 28%, and 7%, respectively. In addition, the disease-free survival of patients with a tumor that demonstrated a high percentage of TSLC1 protein-positive cells was reported to be significantly better than that of patients with a tumor that showed a low percentage of TSLC1 protein-positive cells. CONCLUSIONS: The loss or reduction of TSLC1 expression in resected lung adenocarcinoma cases was associated with a poor prognosis, indicating that TSLC1 represents a central effector gene for controlling the biologic aggressiveness of the tumor and that it is an essential biomarker for predicting patient prognosis. These data may help to detect those patients at high risk for recurrence who might benefit from additional therapeutic strategies such as adjuvant therapy.Sep. 2003, Cancer, 98(5) (5), 1002 - 7, English, International magazine[Refereed]Scientific journal
- Toriello-Carey syndrome associated with respiratory failure and non-mechanical ileus.Toriello-Carey syndrome comprises agenesis of the corpus callosum, telecanthus, small palpebral fissures, Pierre Robin sequence, abnormal ears, and cardiac defects. We report a boy who has some additional findings, including a severe respiratory failure and intestinal dysmotility. The boy died of these two disorders at age 13 months. Histological examination revealed pulmonary immaturity and a defect of smooth muscle cells in the longitudinal muscle coat of the intestinal musculature, both of which might explain some aspects of the pathophysiology of the patient.Aug. 2003, American journal of medical genetics. Part A, 120A(4) (4), 537 - 41, English, International magazine[Refereed]Scientific journal
- Expression of the TSLC1 adhesion molecule in pulmonary epithelium and its down-regulation in pulmonary adenocarcinoma other than bronchioloalveolar carcinoma.TSLC1 (tumor suppressor in lung cancer-1) is an adhesion molecule of the Ig superfamily that binds homophilically and mediates cell-cell interactions. Originally, TSLC1 was cloned as a candidate tumor suppressor from the genomic region that frequently exhibits loss of heterogeneity in human non-small-cell lung cancer (NSCLC). However, there have been no studies on TSLC1 expression in normal lungs or NSCLC. Here we show that pulmonary epithelial cells express TSLC1 and its expression levels are often decreased or lost in primary pulmonary adenocarcinoma, a major histologic type of NSCLC. Immunohistochemistry revealed that TSLC1 was localized at cell-cell boundaries of all columnar epithelial cells in mouse embryonic lungs of 10.5 and 13 days postcoitus. Similar staining patterns were observed in bronchiolar and alveolar epithelial cells of adult human lungs, suggesting a physiologic role for TSLC1 in interactions of these cells. Next we performed Western blot analyses of TSLC1 in 47 primary pulmonary adenocarcinomas and judged each tumor as either decreased or nondecreased by comparing TSLC1 expression levels of the tumor with the levels of normal lungs. The expression profiles had a significant relation to histologic subtypes but not to other clinicopathologic parameters. Sixteen bronchioloalveolar carcinomas (BACs) were all judged nondecreased, while 19 of 31 (63%) adenocarcinomas other than BAC were judged decreased (p < 0.0001). Immunohistochemistry of tumors judged nondecreased revealed that not only BAC cells but also tumor cells in lepidic growth components of adenocarcinomas other than BAC expressed TSLC1 on their lateral plasma membranes. These tumor cells are considered less invasive because they proliferate in a lepidic growth pattern along alveolar walls. Thus, the present results not only support the hypothesis that TSLC1 is a tumor suppressor of NSCLC but also suggest that preserved integrity of TSLC1 may contribute to less invasive phenotypes of lepidic growth tumor cells.Aug. 2003, Laboratory investigation; a journal of technical methods and pathology, 83(8) (8), 1175 - 83, English, International magazine[Refereed]Scientific journal
- SgIGSF: a new mast-cell adhesion molecule used for attachment to fibroblasts and transcriptionally regulated by MITF.Microphthalmia transcription factor (MITF) is a basic-helix-loop-helix-leucine zipper-type transcription factor. The mutant mi and Mi(wh) alleles encode MITFs with deletion and alteration of a single amino acid, respectively, whereas the tg is a null mutation. In coculture with NIH/3T3 fibroblasts, the numbers of cultured mast cells (CMCs) derived from C57BL/6 (B6)(mi/mi), B6(Miwh/Miwh), and B6(tg/tg) mice that adhered to NIH/3T3 fibroblasts were one third as large as the number of B6(+/+) CMCs that adhered to NIH/3T3 fibroblasts. From a cDNA library of B6(+/+) CMCs, we subtracted messenger RNAs expressed by B6(mi/mi) CMCs and found a clone encoding SgIGSF, a recently identified member of the immunoglobulin superfamily. Northern and Western blot analyses revealed that SgIGSF was expressed in B6(+/+) CMCs but not in CMCs derived from MITF mutants. Immunocytochemical analysis showed that SgIGSF localized to the cell-to-cell contact areas between B6(+/+) CMCs and NIH/3T3 fibroblasts. Transfection of B6(mi/mi) and B6(tg/tg) CMCs with SgIGSF cDNA normalized their adhesion to NIH/3T3 fibroblasts. NIH/3T3 fibroblasts did not express SgIGSF, indicating that SgIGSF acts as a heterophilic adhesion molecule. Transfection of B6(tg/tg) CMCs with normal MITF cDNA elevated their SgIGSF expression to normal levels. These results indicated that SgIGSF mediated the adhesion of CMCs to fibroblasts and that the transcription of SgIGSF was critically regulated by MITF.Apr. 2003, Blood, 101(7) (7), 2601 - 8, English, International magazine[Refereed]Scientific journal
- Localization of the PP2A B56gamma regulatory subunit at the Golgi complex: possible role in vesicle transport and migration.The BL6 subline was derived from the F10 line, which was derived from the B16 mouse melanoma cell line. BL6 cells are more invasive than F10 cells and differ genetically from F10 cells by an alteration of the gene encoding the B56gamma regulatory subunit of protein phosphatase 2A (PP2A). This alteration results in the transcription of mRNA encoding a truncated variant of the B56gamma1 isoform (Deltagamma1). When F10 cells were stained with a polyclonal antibody that recognizes three B56gamma isoforms, B56gamma1, B56gamma2, and B56gamma3, the immunofluorescent signals co-localized well with the cis-Golgi marker proteins. When BL6 cells were fractionated in a sucrose gradient, B56gamma1 and B56gamma2, but not B56gamma3, were present in the Golgi-enriched fraction. This fraction also contained the catalytic subunit of PP2A. FLAG-tagged Deltagamma1 preferentially localized to the trans-Golgi area rather than the cis-Golgi. This localization was the same as that of FLAG-tagged B56gamma1. NIH3T3 cells stably expressing Deltagamma1 transported a mutant viral protein from the endoplasmic reticulum to the plasma membrane much faster than wild-type cells. Their directional migration, as assessed by the advance of cells into a cell-free area, was also elevated. As Deltagamma1 reduces the activity of the B56gamma-containing PP2A holoenzymes, these results suggest that the normal holoenzymes suppress vesicle transport and that Deltagamma1 might increase the invasive ability of BL6 cells by activating Golgi function.Lead, Feb. 2003, The American journal of pathology, 162(2) (2), 479 - 89, English, International magazine[Refereed]Scientific journal
- A truncated isoform of the protein phosphatase 2A B56gamma regulatory subunit may promote genetic instability and cause tumor progression.F10, a subline of the B16 mouse melanoma cell line, is itself the parent of the more metastatic BL6 line. BL6 cells differ from F10 cells by an alteration of the gene encoding the B56gamma regulatory subunit of protein phosphatase 2A (PP2A), which results in the expression of a truncated variant of the subunit (Deltagamma1). PP2A is involved in regulating the cell-cycle checkpoint and we found that the checkpoint in BL6 cells is aberrant when the Deltagamma1 protein is expressed. That is, although Deltagamma1 protein levels in cultured BL6 cells are low and these cells do not show an altered checkpoint on gamma-irradiation, irradiated footpad BL6 tumor cells show both a marked increase in Deltagamma1 levels and more extensive polyploidy and less apoptosis than F10 cells. These observations were reproduced with Deltagamma1 gene-transfected F10 cells (F10(Deltagamma1)). Deltagamma1 expression and an aberrant checkpoint are also associated with a higher metastatic ability because irradiated F10(Deltagamma1) tumors metastasized much more frequently than F10 tumors, which rarely metastasized whether irradiated or not. Nonirradiated F10(Deltagamma1) tumors, which do not express Deltagamma1 protein, had similarly low rates of metastasis. The greater metastatic ability of irradiated F10(Deltagamma1) tumors also correlated with the acquisition of many more genomic alterations. Thus, it seems that Deltagamma1 expression may damage the checkpoint, which may then allow the acquisition of genetic alterations that promote metastasis. These observations support the notion that mechanisms promoting the genetic instability of tumors could also aid tumor progression from the nonmetastatic to the metastatic state.Jan. 2003, The American journal of pathology, 162(1) (1), 81 - 91, English, International magazine[Refereed]Scientific journal
- Cancer develops and progresses as genetic alterations occur subsequently. Onset process of cancer has become well understood in some types of cancer, such as colorectal cancers. In this process, responsible alterations were identified in numbers of oncogenes such as k-ras, and tumor suppressor genes such as p53, as Vogelstein proposed earlier in the multistage carcinogenesis theory. In contrast, our understanding remains short to draw such an adequate diagram for the process during which cancer becomes more malignant, i.e., metastatic. To examine the molecular basis for this progression step, mouse metastasis models have been established where tumor cell lines are inoculated into mice and metastasize to specific organs. The model using B16 melanoma cells is one of the most developed. BL6 subline, one of the most metastatic, was obtained from F10 subline simply through six rounds of in vitro selection. Nonetheless, BL6 cells metastasize lungs much more heavily than F10 cells when injected subcutaneously. The difference in gene expression between the two sublines is considered rather small but relevant for spontaneous metastasis. We began our research by elaborating a method for the construction of subtracted cDNA libraries, and made it applicable to BL6 and F10 cells. As a result, we were able to isolate a couple of genes that were expressed differently between the two sublines. As might be expected, each of the genes appeared to play a role more or less in distinct aspects of spontaneous metastasis of B16 melanoma cells. Moreover, similar roles were expected for the genes in the process by which human melanoma cells metastasize.2002, Histology and histopathology, 17(3) (3), 951 - 9, English, International magazine[Refereed]Scientific journal
- Increased expression of a nucleolar Nop5/Sik family member in metastatic melanoma cells: evidence for its role in nucleolar sizing and function.F10 and BL6 cells of B16 mouse melanoma cells are metastatic after intravenous injection, but only BL6 cells can metastasize to lungs after subcutaneous injection. Differences in gene expression between the two cell lines were examined, and a greater expression of the Sik-similar protein (Sik-SP) gene was found in BL6 cells. Structurally, Sik-SP belongs to the nucleolar Nop5/Sik family whose members play central roles in ribosome biogenesis; however, the function of Sik-SP has not been examined. Cytology with green fluorescent protein-fused proteins showed that Sik-SP was localized to the nucleolus. To examine whether Sik-SP is involved in ribosome biogenesis, two parameters were measured: magnitude of ribosomal RNA synthesis per nucleus and magnitude of protein production from the same amount of mRNA of an exogenous luciferase gene. Both values and, in addition, nucleolar size were larger in COS-7 monkey kidney cells overexpressing Sik-SP and BL6 cells than in mock-transfected COS-7 and F10 cells, respectively. Sik-SP seemed to promote ribosome biogenesis in the nucleolus. Furthermore, the expression of Sik-SP seemed to confer a greater cell growth response to serum, because such a response was greater in BL6 cells and F10 cells overexpressing Sik-SP than in untreated and mock-transfected F10 cells. Sik-SP may render melanoma cells more competent to survive through augmenting the activity of nucleolus.Oct. 2001, The American journal of pathology, 159(4) (4), 1363 - 74, English, International magazine[Refereed]Scientific journal
- Inhibitory effect on natural killer activity of microphthalmia transcription factor encoded by the mutant mi allele of mice.The mouse mi locus encodes a basic-helix-loop-helix-leucine zipper-type transcription factor, microphthalmia transcription factor (MITF). Mice of mi/mi genotype express a mutant form of MITF (mi-MITF), whereas mice of tg/tg genotype have a transgene in the 5' flanking region of the mi gene and do not express MITF. Although the mi/mi mouse is deficient in natural killer (NK) activity, it was found that the tg/tg mouse was normal in this respect. To know the cause, spleen cells of both genotypes were compared. Although the proportion of spleen cells expressing an NK cell marker, NK1.1, was comparable in both mice, the proportion of large granular lymphocytes decreased only in mi/mi mice. The difference between mi/mi and tg/tg mice was reproducible in the culture supplemented with interleukin-2. Moreover, the perforin gene expression was reduced in mi/mi-cultured spleen cells. Wild-type (+) MITF transactivated, but mi-MITF suppressed, the perforin gene promoter through the NF-P motif, a strong cis-acting element. However, neither +-MITF nor mi-MITF bound the NF-P motif. Instead, 2 nuclear factors that bound the NF-P motif were retained in the cytoplasm of mi/mi-cultured spleen cells. In addition, overexpression of mi-MITF resulted in cytoplasmic retention of the 2 NF-P motif-binding factors in cytotoxic T lymphocytes. The presence of mi-MITF rather than the absence of +-MITF appeared to lead to poor transactivation of the NF-P motif by intercepting NF-P motif-binding factors. This inhibitory effect of mi-MITF may cause the deficient cytotoxicity of NK cells in mi/mi mice. (Blood. 2001;97:2075-2083)Apr. 2001, Blood, 97(7) (7), 2075 - 83, English, International magazine[Refereed]Scientific journal
- 2024, 肝臓, 65(2) (2)Acetaminophen-induced liver injury with atypical histopathologic findings: a case report[Refereed]
- (一社)日本肝臓学会, Nov. 2023, 肝臓, 64(11) (11), 575 - 582, Japanese[Refereed]
- Japan Society of Hepatology, 01 Mar. 2023, Kanzo, 64(3) (3), 141 - 149[Refereed]
- 2023, 消化器病学サイエンス, 7(4) (4)キーワード No.75 腫瘍関連マクロファージ[Invited]
- Japan Society of Hepatology, 01 Nov. 2021, Kanzo, 62(11) (11), 765 - 769, Japanese[Refereed]Report scientific journal
- [A Case of Laparoscopic Gastric Local Resection for Dedifferentiated Gastric Liposarcoma].A 73 year-old-woman visited our emergency department with a sudden stomach ache. A 7 cm tumor was found on the greater curvature side of the stomach by contrast-enhanced CT, and showed mosaic pattern when visualized with a contrast agent. An esophagogastroduodenoscopy showed normal mucosal gastric surface with compression findings by the gastric submucosal tumor, and therefore she was admitted to our department for surgery. Abdominal ultrasound revealed an uneven gastric submucosal tumor containing cystic components with a clear border, and gastric GIST was suspected due to its appearance, and therefore, laparoscopic gastric local resection was performed. The gastric tumor was located on the dorsal side of the greater curvature and adhered highly to the retroperitoneum and spleen. The omental incision was conducted first, and the adhesion around the tumor was carefully detached, following which wedge resection was performed using Endo-GIA®at the base of the tumor. The pathological findings of the resected specimens were mainly spindle-shaped tumor cells rich in polymorphism with a high degree of necrosis, and did not seem to be conclusively GIST; as such, various immunological tests were performed.c -kit(-), DOG-1(-), S-100 p(-), desmin(-), a-SMA(focal+), p16(+), MDM2(+), CDK4(+) results led to the diagnosis of dedifferentiated liposarcoma. The patient is currently being followed up with and is alive without recurrence 10 months after the operation.Dec. 2019, Gan to kagaku ryoho. Cancer & chemotherapy, 46(13) (13), 2204 - 2206, Japanese, Domestic magazine
- Jul. 2016, CANCER RESEARCH, 76, EnglishSummary international conference
- Sep. 2015, EUROPEAN JOURNAL OF CANCER, 51, S20 - S20, EnglishContribution of cancer-associated fibroblasts and M2-polarized macrophages to neuroblastoma developmentSummary international conference
- (一社)日本病理学会, Jul. 2013, 診断病理, 30(3) (3), 211 - 216, Japanese[Refereed]
- (一社)日本病理学会, Apr. 2013, 診断病理, 30(2) (2), 104 - 107, Japanese[Refereed]
- 日本臨床外科学会, Apr. 2011, 日本臨床外科学会雑誌, 72(4) (4), 965 - 971, Japanese悪性腫瘍との鑑別が困難であった肝硬化性血管腫の1例[Refereed]
- (一社)日本病理学会, Jan. 2011, 診断病理, 28(1) (1), 73 - 76, Japanese膀胱原発悪性血管周囲類上皮細胞腫瘍の1例[Refereed]
- Japan Society for Bioscience, Biotechnology, and Agrochemistry, 2004, KAGAKU TO SEIBUTSU, 42(5) (5), 313 - 321, Japanese[Invited]Introduction scientific journal
- 2002, 化学と生物, 40(9) (9), 567 - 569タンパク質脱リン酸化酵素と癌細胞の悪性化[Invited]Introduction scientific journal
- Contributor, Chapter10『臓器別疾患』Ⅵ「上部消化管（食道・胃）の疾患」, 医歯薬出版株式会社, May 2024歯学生のための基礎病理学
- Joint work, 金芳堂, May 2019, Japanese免疫染色究極マニュアル 診断編 10 大腸Scholarly book
- Joint work, 北隆館, Sep. 2017, Japanese別冊BIO Clinica. 消化管の慢性炎症 / 食道扁平上皮癌の進展や発がん初期段階におけるマクロファージの解析Scholarly book
- Joint work, 北隆館, Feb. 2016, Japanese別冊BIO Clinica 慢性炎症と疾患 / がん微小環境とがんの増殖・浸潤・転移 消化管がんの進展とがん間質Scholarly book
- 第114回日本病理学会総会・学術集会, Apr. 2025食道扁平上皮癌と癌関連線維芽細胞との直接共培養により発現誘導されるISG15の解析
- 第114回日本病理学会総会・学術集会, Apr. 2025大腸癌の進展に伴うがん関連線維芽細胞の不均一性の解明
- 第114回日本病理学会総会・学術集会, Apr. 2025経過中に肉芽腫性炎症を生じ診断に難渋した眼窩内脂肪肉腫の一例
- 第114回日本病理学会総会・学術集会, Apr. 2025食道扁平上皮癌細胞と共培養した癌関連線維芽細胞において発現亢進するビグリカンの解析
- 第114回日本病理学会総会・学術集会, Apr. 2025癌関連線維芽細胞との相互作用により食道扁平上皮癌において発現亢進するBST2の機能解析
- 第114回日本病理学会総会・学術集会, Apr. 2025マクロファージと肝細胞癌との間接共培養で発現上昇するCHI3L1とOPNの機能解析
- 第114回日本病理学会総会・学術集会, Apr. 2025膵上皮内癌・微小浸潤癌の腫瘍免疫微小環境に関する免疫組織化学的検討
- 第114回日本病理学会総会・学術集会, Apr. 2025癌関連線維芽細胞との相互作用によって癌細胞において発現亢進するAREGは食道扁平上皮癌の進展を促進する
- 第114回日本病理学会総会・学術集会, Apr. 2025pT1/T2舌癌において骨髄由来間葉系幹細胞は癌細胞との相互作用によりiCAF様形質を獲得する
- 第35回日本消化器癌発生学会総会, Nov. 2024癌関連線維芽細胞と直接共培養した食道扁平上皮癌細胞において発現亢進するアンフィレグリンは癌進展を促進する
- 第83回日本癌学会学術総会, Sep. 2024腫瘍関連マクロファージとの相互作用によって誘導されるYKL40/integrin β4経路は卵巣癌の進展に寄与する
- 第44回日本分子腫瘍マーカー研究会, Sep. 2024癌細胞とマクロファージとの相互作用によって活性化する CCL2/CCR2 経路は肝細胞癌の進展を促進する
- 第44回日本分子腫瘍マーカー研究会, Sep. 2024ポドプラニンは大腸発癌早期の陰窩周囲線維芽細胞に発現する腫瘍マーカーである
- 第20回日本病理学会カンファレンス, Jul. 2024ポドプラニン陽性癌関連線維芽細胞は大腸発癌早期に出現する
- 第41回 分子病理学研究会, Jul. 2024間質細胞との相互作用による食道癌進展機構の解析[Invited]Invited oral presentation
- 第41回 分子病理学研究会, Jul. 2024QuPathとCNNモデルを用いた機械学習によるTranswell migration assayの効率化
- The 8th Japanese Cancer Association (JCA)-American Association for Cancer Research (AACR) Special Joint Conference, Jun. 2024The heterogeneity of cancer-associated fibroblasts in pT1/T2 tongue squamous cell carcinoma
- 第113回日本病理学会総会・学術集会, Mar. 2024舌癌細胞とマクロファージの相互作用におけるP. gingivalis由来LPSの影響
- 第113回日本病理学会総会・学術集会, Mar. 2024食道扁平上皮癌と癌関連線維芽細胞との直接共培養により発現誘導される ISG15の解析
- 第113回日本病理学会総会・学術集会, Mar. 2024卵巣癌と腫瘍関連マクロファージの相互作用により誘導されたYKL40は癌の進展に関与する
- 第113回日本病理学会総会・学術集会, Mar. 2024肝細胞癌とマクロファージの間接共培養系において上昇が確認されたサイトカインの解析
- 第113回日本病理学会総会・学術集会, Mar. 2024病理解剖により肺腫瘍血栓性微小血管症と診断した5症例の臨床病理学的検討
- 第113回日本病理学会総会・学術集会, Mar. 2024ヒト食道扁平上皮癌組織免疫染色画像の疑似蛍光カラー解析
- 第113回日本病理学会総会・学術集会, Mar. 2024pT1/T2舌扁平上皮癌におけるがん関連線維芽細胞の不均一性
- 第113回日本病理学会総会・学術集会, Mar. 2024食道扁平上皮癌細胞とマクロファージの相互作用は癌細胞にIFI16とIL-1α の発現を誘導し、癌を進展させる
- 第113回日本病理学会総会・学術集会, Mar. 2024癌関連線維芽細胞由来のperiostinは癌細胞や間質細胞の運動能亢進を介して食道扁平上皮癌の進展を促進する
- 第113回日本病理学会総会・学術集会, Mar. 2024食道扁平上皮癌の進展における癌細胞とマクロファージの直接接触を介した相互作用の重要性
- 第113回日本病理学会総会・学術集会, Mar. 2024癌関連線維芽細胞との相互作用により食道扁平上皮癌において発現亢進するBST2の機能解析
- 第113回日本病理学会総会・学術集会, Mar. 2024食道扁平上皮癌細胞と共培養した癌関連線維芽細胞において発現亢進するビグリカンの解析
- 第113回日本病理学会総会・学術集会, Mar. 2024癌関連線維芽細胞と共培養した食道扁平上皮癌細胞において発現亢進するア ンフィレグリンの解析
- 第34回日本消化器癌発生学会総会, Nov. 2023食道扁平上皮癌と腫瘍関連マクロファージとの直接共培養により発現亢進する IFI16 はIL-1αの分泌を介して腫瘍進展に関与するPoster presentation
- 第82回日本癌学会学術総会, Sep. 2023Analysis of interactions between carcinoma cells and macrophages in the progression of hepatocellular carcinomaPoster presentation
- 第82回日本癌学会学術総会, Sep. 2023LPS from periodontal pathogen P.gingivalis enhances interplay of tongue cancer cell with macrophage via TLR4Poster presentation
- 第82回日本癌学会学術総会, Sep. 2023Analysis of interactions between carcinoma cells and tumor-associated macrophages in the progression of ovarian cancerPoster presentation
- 第82回日本癌学会学術総会, Sep. 2023IFI16 induced by direct co-culture between ESCC cell and macrophage promotes tumor progression via secretion of IL-1αPoster presentation
- 第82回日本癌学会学術総会, Sep. 2023Periostin derived from CAFs in ESCC microenvironment promotes cancer progressionPoster presentation
- 第82回日本癌学会学術総会, Sep. 2023Analysis of amphiregulin upregulated in ESCC cells directly co-cultured with cancer-associated fibroblastsPoster presentation
- 第82回日本癌学会学術総会, Sep. 2023Using 3D cell culture system to assess the roles of CAFs in ESCC microenvironmentPoster presentation
- 第82回日本癌学会学術総会, Sep. 2023The significance of osteopontin/YKL-40-integrin β4-p70S6K axis in early esophageal squamous cell carcinomaPoster presentation
- 第82回日本癌学会学術総会, Sep. 2023MMP9 and IL-8 are induced in ESCC cells by interaction with macrophages and thereby promoting cancer cell invasionOral presentation
- 第43回日本分子腫瘍マーカー研究会, Sep. 2023食道扁平上皮癌微小環境において癌関連線維芽細胞由来のペリオスチンが癌進展を促進するOral presentation
- 第19回 日本病理学会カンファレンス, Aug. 2023免疫細胞ヒト化マウスを用いた食道扁平上皮癌微小環境の解析Poster presentation
- 第112回日本病理学会総会, Apr. 2023食道扁平上皮癌と癌関連線維芽細胞の直接共培養により発現誘導され る ISG15 の解析
- 第112回日本病理学会総会, Apr. 2023３次元細胞培養担体を用いた食道扁平上皮癌微小環境における癌関連 線維芽細胞の機能解析
- 第112回日本病理学会総会, Apr. 2023歯周病原細菌由来 LPS は舌癌細胞の TLR4 を介してマクロファージと の相互作用を増強する
- 第112回日本病理学会総会, Apr. 2023食道扁平上皮癌と腫瘍関連マクロファージとの直接共培養により発現 が誘導される IFI16 の機能解析
- 第112回日本病理学会総会, Apr. 2023腫瘍関連マクロファージとの共培養により ESCC で発現低下する miR132-5p は癌細胞の運動・浸潤能を促進する
- 第112回日本病理学会総会, Apr. 2023マクロファージとの相互作用によって癌細胞に誘導される IL-7R の食道 扁平上皮癌の進展における役割
- 第112回日本病理学会総会, Apr. 2023癌関連線維芽細胞と直接共培養した食道扁平上皮癌細胞において発現 が亢進する遺伝子の解析
- 第112回日本病理学会総会, Apr. 2023食道扁平上皮癌との直接共培養系によって作成した癌関連線維芽細胞において発現亢進する遺伝子の解析
- 第112回日本病理学会総会, Apr. 2023直腸癌術後の人工肛門造設部に発生した胎児型形質を伴う癌の一例
- 第112回日本病理学会総会, Apr. 2023マクロファージとの相互作用は食道扁平上皮癌細胞に MMP9 の発現を 誘導し、IL-8 と協調して癌を進展させる
- 第112回日本病理学会総会, Apr. 2023早期食道扁平上皮癌における YKL-40/osteopontin-ITG β 4-p70S6K 経路の意義
- 第112回日本病理学会総会, Apr. 2023強膜開窓生検にて診断し得た脈絡膜 Mesectodermal leiomyoma の 一例
- 第112回日本病理学会総会, Apr. 2023pT1/T2 舌扁平上皮癌リンパ節転移におけるがん関連線維芽細胞の役割
- 第112回日本病理学会総会, Apr. 2023肝細胞癌における腫瘍関連マクロファージの機能解析
- 第２回日本医学会連合 Rising Star リトリート, Mar. 2023間質細胞との細胞間相互作用による食道癌の進展機構の解析[Invited]
- 第99回日本病理学会近畿支部学術集会, Dec. 2022眼球内腫瘍の一例
- 第33回日本消化器癌発生学会総会, Nov. 2022マクロファージとの直接共培養で食道扁平上皮癌において発現亢進するIL-7Rは癌細胞の生存・増殖能や運動能を亢進させる
- 第81回日本癌学会学術総会, Sep. 2022食道扁平上皮癌と腫瘍関連マクロファージとの直接共培養により発現が亢進されるIFI16の解析
- 第81回日本癌学会学術総会, Sep. 2022腫瘍関連マクロファージとの共培養によりESCCで発現低下するmiR-132-5pは癌細胞の運動能・浸潤能に関与する
- 第81回日本癌学会学術総会, Sep. 2022食道扁平上皮癌と癌関連線維芽細胞の直接共培養系の解析
- 第81回日本癌学会学術総会, Sep. 2022マクロファージとの相互作用で誘導されるOPN/YKL-40-ITGβ4-p70S6K経路は食道扁平上皮初期発癌に関与する
- 第81回日本癌学会学術総会, Sep. 2022マクロファージとの直接共培養によって食道扁平上皮癌において発現上昇するInterleukin 7 receptor（IL-7R）の機能解析
- 第81回日本癌学会学術総会, Sep. 2022マクロファージとの直接接着は食道扁平上皮癌細胞内のSTAT3-MMP9 axisを活性化し、その浸潤能を亢進させる
- 第81回日本癌学会学術総会, Sep. 2022口腔悪性黒色腫における腫瘍関連マクロファージの意義に関する病理学的検討
- 第81回日本癌学会学術総会, Sep. 2022pT1-T2舌扁平上皮癌リンパ節転移における癌細胞と線維芽細胞の相互作用
- The 81st Annual Meeting of the Japanese Cancer Association, Sep. 2022The significance of tumor-associated macrophages in oral melanoma
- 第42回日本分子腫瘍マーカー研究会, Sep. 2022マクロファージとの相互作用で誘導されるYKL-40/osteopontin-integrin beta4-p70S6K経路は食道扁平上皮初期発癌に関与する
- 第18回日本病理学会カンファレンス, Jul. 2022Direct contact with MΦs activates STAT3-MMP9 axis in ESCC cells and promotes their invasiveness
- 第31回日本がん転移学会学術集会・総会, Jul. 2022マクロファージとの直接接触はSTAT3-MMP9系を介して食道扁平上皮癌細胞の運動・浸潤能を促進させる
- 第111回日本病理学会総会, Apr. 2022舌癌細胞／マクロファージ相互作用に対する歯周病原細菌由来lipopolysaccharideの影響
- 第111回日本病理学会総会, Apr. 2022３次元細胞培養担体を用いた食道扁平上皮癌微小環境におけるマクロ ファージの機能解析
- 第111回日本病理学会総会, Apr. 2022腫瘍関連マクロファージとの共培養によりESCCで発現低下するmiR132-5pは癌細胞の運動能・浸潤能に関与する
- 第111回日本病理学会総会, Apr. 2022対側鼠径リンパ節に転移した稀な乳癌（三重癌）の一例
- 第111回日本病理学会総会, Apr. 2022癌関連線維芽細胞および癌細胞で発現する Metallothionein 2A は食道扁平上皮癌の進展に関与する
- 第111回日本病理学会総会, Apr. 2022食道扁平上皮癌と腫瘍関連マクロファージとの直接共培養により誘導される IFI16 の評価
- 第111回日本病理学会総会, Apr. 2022マクロファージとの直接共培養によって食道扁平上皮癌において活性 化される IL-7/IL-7R 経路の機能解析
- 第111回日本病理学会総会, Apr. 2022食道扁平上皮初期発癌におけるマクロファージの機能解析
- 第111回日本病理学会総会, Apr. 2022口腔の発癌過程においてマクロファージの上皮内集簇により誘導されるCCL20の役割
- 第111回日本病理学会総会, Apr. 2022剖検講習会「病理解剖報告書およびフローチャートの作成について」[Invited]Public discourse
- 第111回日本病理学会総会, Apr. 2022舌扁平上皮癌リンパ節転移における癌細胞と線維芽細胞の相互作用
- 第111回日本病理学会総会, Apr. 2022S100A8/A9 は Akt および p38 MAPK を介して食道扁平上皮癌細胞 の運動・浸潤能を亢進させる
- 第111回日本病理学会総会, Apr. 2022マクロファージとの直接接触は STAT3-MMP9 系を介して食道扁平上 皮癌細胞の運動・浸潤能を促進させる
- 第18回日本消化管学会総会学術集会, Feb. 2022, Japanese癌関連線維芽細胞および癌細胞で発現するMetallothionein 2Aは食道扁平上皮癌の進展に関与する[Invited]Nominated symposium
- 第18回日本消化管学会総会学術集会, Feb. 2022, Japaneseマクロファージとの相互作用により発現誘導されるS100A8/A9はAkt、p38を介して食道扁平上皮癌細胞の運動能、浸潤能を亢進させる[Invited]Nominated symposium
- 第 32 回日本消化器癌発生学会総会・第 10 回国際消化器癌発生会議, Nov. 2021, JapaneseCCL1 derived from TAMs contributes to ESCC progression via CCR8-mediated Akt/PRAS40/mTOR pathway[Invited]Invited oral presentation
- 第 32 回日本消化器癌発生学会総会・第 10 回国際消化器癌発生会議, Nov. 2021, JapaneseMT2A expressed in CAFs and cancer cells promotes ESCC progressionPoster presentation
- 第67回日本病理学会秋期特別総会, Nov. 2021The roles of cell–cell interactions between tumor cells and stromal cells in tumor progression (Lecture A)[Invited]Invited oral presentation
- 第80回日本癌学会学術総会, Oct. 2021食道扁平上皮癌と腫瘍関連マクロファージとの直接共培養により誘導される遺伝子群の解析Poster presentation
- 第80回日本癌学会学術総会, Oct. 2021pT1またはpT2舌扁平上皮癌の頸部リンパ節転移における線維芽細胞の重要性Poster presentation
- 第80回日本癌学会学術総会, Oct. 2021マクロファージとの相互作用により誘導される舌癌由来CCL20はマクロファージのCD163発現を促進するPoster presentation
- 第80回日本癌学会学術総会, Sep. 2021食道扁平上皮癌の発癌初期段階における癌関連線維芽細胞の解析Poster presentation
- 第80回日本癌学会学術総会, Sep. 2021癌関連線維芽細胞においてMT2Aにより発現が調整されるIGFBP2は食道扁平上皮癌細胞の運動、浸潤能を亢進させるPoster presentation
- 第80回日本癌学会学術総会, Sep. 2021マクロファージとの直接接着環境は食道扁平上皮癌細胞からのMMP9分泌を誘導し、その浸潤能を亢進させるPoster presentation
- 第80回日本癌学会学術総会, Sep. 2021食道扁平上皮発癌の初期段階におけるマクロファージの機能解析Poster presentation
- 第80回日本癌学会学術総会, Sep. 2021マクロファージとの直接共培養によって食道扁平上皮癌において発現上昇するS100A8/A9の機能解析Poster presentation
- 第41回日本分子腫瘍マーカー研究会, Sep. 2021マクロファージとの相互作用により食道扁平上皮癌において発現誘導されるS100A8/A9はAktおよびp38MAPK経路を介して癌細胞の運動能、浸潤能を亢進させるOral presentation
- 第17回日本病理学会カンファレンス, Aug. 2021マクロファージとの直接接触は食道扁平上皮癌細胞からのMMP9分泌亢進を介して運動・浸潤能を促進させるPoster presentation
- 第17回日本病理学会カンファレンス, Aug. 2021腫瘍関連マクロファージはCCL3-CCR5系を介して食道扁平上皮癌の進展に寄与するPoster presentation
- 第30回日本がん転移学会学術集会・総会, Jul. 2021線維芽細胞はpT1, pT2舌扁平上皮癌の頸部リンパ節転移に関与するPoster presentation
- 第30回日本がん転移学会学術集会・総会, Jul. 2021舌癌の進展における癌細胞／マクロファージ相互作用の変化Poster presentation
- 第110回日本病理学会総会, Apr. 2021腫瘍関連マクロファージ由来のCCL1はCCR8を介して食道扁平上皮癌の運動、浸潤能を亢進させるOral presentation
- 第110回日本病理学会総会, Apr. 2021乳房の有痛性腫瘤として発症した悪性Glomus tumorの一例Poster presentation
- 第110回日本病理学会総会, Apr. 2021食道扁平上皮発癌の初期段階におけるマクロファージの機能解析Poster presentation
- 第110回日本病理学会総会, Apr. 2021癌関連線維芽細胞においてMT2Aにより発現が誘導されるIGFBP2は食道癌細胞の運動、浸潤能を亢進させるPoster presentation
- 第110回日本病理学会総会, Apr. 2021食道扁平上皮癌と腫瘍関連マクロファージとの直接共培養により誘導される遺伝子群の解析Poster presentation
- 第110回日本病理学会総会, Apr. 2021マクロファージとの直接共培養によって食道扁平上皮癌において発現上昇するS100A8/A9の機能解析Poster presentation
- 第110回日本病理学会総会, Apr. 2021舌扁平上皮癌pT1、pT2症例の頸部リンパ節転移における線維芽細胞の重要性Poster presentation
- 第110回日本病理学会総会, Apr. 2021マクロファージに着目した口腔発癌における癌・間質相互作用の解析Poster presentation
- 第27回肝血流動態・機能イメージ研究会, Jan. 2021分子標的薬治療により画像上濃染消失像を呈したHCCの病理組織学的検討Oral presentation
- 第31回日本消化器癌発生学会, Nov. 2020腫瘍関連マクロファージ由来のCCL1はCCR8を介して食道扁平上皮癌の運動能・浸潤能を亢進させるOral presentation
- 第31回日本消化器癌発生学会, Nov. 2020癌関連線維芽細胞はPAI-1の分泌を介して食道扁平上皮癌の進展に寄与するOral presentation
- 第79回日本癌学会学術総会, Oct. 2020舌白板症における上皮内CD163陽性マクロファージは悪性スクリーニングの有望なツールであるPoster presentation
- 第79回日本癌学会学術総会, Oct. 2020マクロファージとの直接共培養によって食道扁平上皮癌において発現上昇するS100A8/A9の機能解析Poster presentation
- 第79回日本癌学会学術総会, Oct. 2020腫瘍関連マクロファージは食道扁平上皮癌のmiR-132-5pの発現を抑制し、Akt/PRAS40/mTOR経路を介して運動・浸潤能を亢進させるPoster presentation
- 第79回日本癌学会学術総会, Oct. 2020腫瘍関連マクロファージ由来のCCL1はCCR8を介して食道扁平上皮癌の運動能・浸潤能を亢進させるPoster presentation
- 第79回日本癌学会学術総会, Oct. 2020食道扁平上皮癌の発癌初期段階における癌関連線維芽細胞の解析Poster presentation
- 第79回日本癌学会学術総会, Oct. 2020食道扁平上皮癌微小環境における癌関連線維芽細胞で高発現するMT2Aの機能解析Poster presentation
- 第79回日本癌学会学術総会, Oct. 2020癌関連線維芽細胞はPAI-1を分泌することで食道扁平上皮癌細胞とマクロファージの遊走能および浸潤能を促進するOral presentation
- 第79回日本癌学会学術総会, Oct. 2020, English腫瘍関連マクロファージはCCL3-CCR5系を介して食道扁平上皮癌の遊走能と浸潤能を亢進するOral presentation
- 第40回日本分子腫瘍マーカー研究会, Sep. 2020CCL1-CCR8経路はAkt/PRSAS40/mTORシグナルを介して食道扁平上皮癌の進展を促進するOral presentation
- 第80回兵庫神経内科研究会, Aug. 2020意識障害・けいれんを来した82歳担癌男性例Oral presentation
- 第29回日本がん転移学会総会・学術集会, Jul. 2020食道扁平上皮癌微小環境における癌関連線維芽細胞で高発現するMT2Aの機能解析Poster presentation
- 第29回日本がん転移学会総会・学術集会, Jul. 2020食道扁平上皮癌の発癌初期段階における癌関連線維芽細胞の解析Poster presentation
- 第29回日本がん転移学会総会・学術集会, Jul. 2020食道扁平上皮癌細胞と腫瘍関連マクロファージとの直接接触により発現変化する遺伝子群の解析Poster presentation
- 第29回日本がん転移学会総会・学術集会, Jul. 2020腫瘍関連マクロファージは食道扁平上皮癌のmiR-29c 発現抑制ならびにGABRP発現亢進によって運動能を促進するPoster presentation
- 第29回日本がん転移学会総会・学術集会, Jul. 2020口腔癌の発生におけるCD163陽性マクロファージの解析Poster presentation
- 第29回日本がん転移学会総会・学術集会, Jul. 2020癌関連線維芽細胞はPAI-1 の分泌を介して食道扁平上皮癌の進展に寄与するPublic symposium
- 第29回日本がん転移学会総会・学術集会, Jul. 2020腫瘍関連マクロファージと食道扁平上皮癌細胞はCCL3-CCR5 系を介して癌の進展に寄与するPublic symposium
- 第29回日本がん転移学会総会・学術集会, Jul. 2020食道扁平上皮癌と腫瘍関連マクロファージとの相互作用はCCL1/CCR8 経路の活性化を介して癌進展に関与するPublic symposium
- 第109回日本病理学会総会, Jul. 2020食道扁平上皮癌微小環境中の腫瘍関連マクロファージはIL-1Raを分泌するPoster presentation
- 第109回日本病理学会総会, Jul. 2020緩徐に進行する複視にて発症した眼窩内solitary fibrous tumorの一例Poster presentation
- 第109回日本病理学会総会, Jul. 2020口腔の発癌段階におけるCD163陽性マクロファージの解析Oral presentation
- 第109回日本病理学会総会, Jul. 2020食道扁平上皮癌微小環境における癌関連線維芽細胞で高発現する遺伝子群の解析Poster presentation
- 第109回日本病理学会総会, Jul. 2020食道扁平上皮癌の発癌初期段階における癌関連線維芽細胞の解析Poster presentation
- 第109回日本病理学会総会, Jul. 2020食道扁平上皮癌細胞と腫瘍関連マクロファージとの直接接触により発現変化する遺伝子群の解析Poster presentation
- 第109回日本病理学会総会, Jul. 2020マクロファージとの直接接触は食道扁平上皮癌細胞からのMMP9分泌亢進を介して運動・浸潤能を促進させるPoster presentation
- 第109回日本病理学会総会, Jul. 2020腫瘍関連マクロファージとの共培養により食道扁平上皮癌細胞で発現低下するmiR-132-5pの解析Poster presentation
- 第109回日本病理学会総会, Jul. 2020腫瘍関連マクロファージは食道扁平上皮癌のmiR-29c発現抑制ならびにGABRP発現亢進によって運動能を促進するPoster presentation
- 第109回日本病理学会総会, Jul. 2020癌関連線維芽細胞はPAI-1の分泌を介して食道扁平上皮癌の進展に寄与するOral presentation
- 第109回日本病理学会総会, Jul. 2020腫瘍関連マクロファージはCCL3-CCR5系を介して食道扁平上皮癌の進展に寄与するOral presentation
- 第30回日本消化器癌発生学会総会, Nov. 2019食道扁平上皮癌と腫瘍関連マクロファージの相互作用は癌進展に関与する[Invited]Nominated symposium
- 第30回日本消化器癌発生学会総会, Nov. 2019腫瘍関連マクロファージとの共培養により食道扁平上皮癌細胞で発現低下するmiR-132-5pの解析Poster presentation
- 第78回日本癌学会学術総会, Sep. 2019癌関連線維芽細胞はPAI-1の分泌を介して食道扁平上皮癌の進展に寄与するPoster presentation
- 第78回日本癌学会学術総会, Sep. 2019生検標本における上皮内CD163陽性マクロファージは舌白板症の鑑別診断に有用であるPoster presentation
- 第78回日本癌学会学術総会, Sep. 2019食道扁平上皮癌微小環境における癌関連線維芽細胞で高発現する遺伝子群の解析Poster presentation
- 第78回日本癌学会学術総会, Sep. 2019食道扁平上皮癌の進展における癌細胞と腫瘍関連マクロファージの直接接触による細胞間相互作用の解析Poster presentation
- 第78回日本癌学会学術総会, Sep. 2019食道扁平上皮癌と腫瘍関連マクロファージとの相互作用は癌進展に関与するPoster presentation
- 第78回日本癌学会学術総会, Sep. 2019腫瘍関連マクロファージはCCL3-CCR5系を介して食道扁平上皮癌の遊走能と浸潤能を亢進するPoster presentation
- 第78回日本癌学会学術総会, Sep. 2019腫瘍関連マクロファージとの共培養により食道扁平上皮癌細胞で発現低下するmiR-132-5pの解析Poster presentation
- 第39回日本分子腫瘍マーカー研究会, Sep. 2019癌関連線維芽細胞はPAI-1の分泌を介して食道扁平上皮癌の進展に寄与するOral presentation
- 第16回日本病理学会カンファレンス, Aug. 2019腫瘍関連マクロファージはCCL3-CCR5系を介して食道扁平上皮癌の進展に寄与するPoster presentation
- 第28回日本がん転移学会学術集会・総会, Jul. 2019食道扁平上皮癌微小環境におけるFAP陽性癌関連線維芽細胞の役割Poster presentation
- 第28回日本がん転移学会学術集会・総会, Jul. 2019腫瘍関連マクロファージはCCL3-CCR5系を介して食道扁平上皮癌の遊走能と浸潤能を亢進するPoster presentation
- 藤川 正隆, 児玉 貴之, 坂本 浩輝, 東野 展英, 小平 日実子, 市原 有美, 西尾 真理, 重岡 学, 狛 雄一朗, 横崎 宏, Jul. 2019腫瘍関連マクロファージとの共培養により食道扁平上皮癌細胞で発現低下するmiR-132-5pの解析Poster presentation
- 第28回日本がん転移学会学術集会・総会, Jul. 2019口腔癌の発癌初期段階におけるCD163陽性マクロファージの意義Poster presentation
- 第28回日本がん転移学会学術集会・総会, Jul. 2019食道扁平上皮癌の進展における癌細胞と腫瘍関連マクロファージの直接接着による細胞間相互作用の解析Poster presentation
- 第28回日本がん転移学会学術集会・総会, Jul. 2019癌関連線維芽細胞はPAI-1の分泌を介して食道扁平上皮癌の進展に寄与するPoster presentation
- 第38回日本分子病理学研究会, Jul. 2019, Japanese, 兵庫県, Domestic conference舌白板症においてCD163陽性マクロファージはIL-10の発現を誘導するPoster presentation
- 第38回日本分子病理学研究会, Jul. 2019, Japanese, 兵庫県, Domestic conference生検標本における上皮内CD163陽性マクロファージは舌白板症の鑑別診断に有用であるPoster presentation
- 第108回日本病理学会総会, May 2019食道がんの進展における癌-間質相互作用の役割[Invited]Nominated symposium
- 第108回日本病理学会 総会・学術大会, May 2019, Japanese, 東京, Domestic conferenceCD163陽性マクロファージに着目した舌白板症の病理組織学的評価Public symposium
- 日本消化器癌発生学会特別研究推進 理事長直轄プロジェクト 「腫瘍-間質相互作用を標的とした癌進展メカニズムの解明」, Feb. 2019, Japanese, 徳島市, Domestic conference食道がんの進展におけるがん-間質相互作用の役割Public discourse
- 第2回神戸理研・神戸大学合同シンポジウム -Development and Disease-, Jan. 2019, English, 神戸理研・神戸大学, 神戸市, Domestic conferenceRole of cancer-stromal interaction in the progression of esophageal cancer[Invited]Nominated symposium
- 第29回日本消化器癌発生学会総会, Nov. 2018, Japanese, 日本消化器癌発生学会, 東京都, Domestic conference食道扁平上皮癌微小環境におけるFAP陽性癌関連線維芽細胞の役割Poster presentation
- 第29回日本消化器癌発生学会総会, Nov. 2018, Japanese, 日本消化器癌発生学会, 東京都, Domestic conference食道扁平上皮癌と腫瘍関連マクロファージとの相互作用はCCL2/CCR2経路の活性化を介して癌進展に関与するOral presentation
- 第6回 神緑会 Young Investigator Award 発表会, Oct. 2018, Japanese, 神戸, Domestic conference食道扁平上皮癌微小環境におけるCyr61の重要性Oral presentation
- 第36回日本脳腫瘍病理学会学術集会, Sep. 2018, Japanese, 日本脳腫瘍病理学会, 東京都, Domestic conference膠芽腫内腫瘍関連マクロファージが膠芽腫細胞に与える影響Oral presentation
- 第77回日本癌学会学術総会, Sep. 2018, Japanese, 日本癌学会, 大阪市, Domestic conference免疫染色画像解析ソフトウェアを用いた食道扁平上皮癌組織免疫染色画像のマクロファージ形態計測Poster presentation
- 第77回日本癌学会学術総会, Sep. 2018, Japanese, Domestic conference食道扁平上皮癌微小環境における癌関連線維芽細胞で高発現する遺伝子群の解析Poster presentation
- 第77回日本癌学会学術集会, Sep. 2018, Japanese, 日本癌学会, 大阪, Domestic conference食道扁平上皮癌微小環境におけるFAP陽性癌関連線維芽細胞の役割Oral presentation
- 第77回日本癌学会学術総会, Sep. 2018, Japanese, 日本癌学会, 大阪市, Domestic conference食道扁平上皮癌微小環境におけるFAP陽性癌関連線維芽細胞の役割Oral presentation
- 第82回日本病理学会近畿支部学術集会, Sep. 2018, Japanese, 日本病理学会近畿支部, 京都市, Domestic conference上皮成分を有する左房内腫瘍の一例Oral presentation
- 第77回日本癌学会学術集会, Sep. 2018, Japanese, 日本癌学会, 大阪, Domestic conference腫瘍関連マクロファージは食道扁平上皮癌のmiR-29cの発現抑制を介してGABRPの発現を亢進させ腫瘍の運動能を促進するPoster presentation
- 第77回日本癌学会学術総会, Sep. 2018, Japanese, 大阪, Domestic conference腫瘍関連マクロファージは食道扁平上皮癌のmiR-29cの発現抑制を介してGABRPの発現を亢進させ腫瘍の運動能を促進するPoster presentation
- 第77回日本癌学会学術集会, Sep. 2018, Japanese, 日本癌学会, 大阪, Domestic conference腫瘍関連マクロファージとの共培養により食道扁平上皮癌細胞で発現低下するマイクロRNAの解析Poster presentation
- 第77回日本癌学会学術総会, Sep. 2018, Japanese, 日本癌学会, 大阪市, Domestic conference腫瘍関連マクロファージとの共培養により食道扁平上皮癌細胞で発現低下するマイクロRNAの解析Poster presentation
- 第77回日本癌学会学術総会, Sep. 2018, Japanese, 日本癌学会, 大阪市, Domestic conference腫瘍関連マクロファージから分泌されるCCL3はAktおよびERK経路を介して食道扁平上皮癌の運動能を亢進するPoster presentation
- 第77回日本癌学会学術総会, Sep. 2018, Japanese, 大阪, Domestic conference腫瘍関連マクロファージから分泌されるCCL3はAktおよびERK経路を介して食道扁平上皮癌の運動能を促進するPoster presentation
- 第77回日本癌学会学術集会, Sep. 2018, Japanese, 日本癌学会, 大阪, Domestic conference口腔癌の発癌初期段階におけるマクロファージの役割Poster presentation
- 第77回日本癌学会学術総会, Sep. 2018, English, 大阪, Domestic conference口腔癌の発癌初期段階におけるマクロファージの役割Oral presentation
- 第77回日本癌学会学術総会, Sep. 2018, Japanese, 日本癌学会, 大阪市, Domestic conferenceマクロファージと食道扁平上皮細胞との相互作用によってG-CSF経路が促進するPoster presentation
- 第15回日本病理学会カンファレンス, Aug. 2018, Japanese, 日本病理学会, 犬山市, Domestic conference腫瘍関連マクロファージから分泌されるCCL3はAktおよびERK経路を介して食道扁平上皮癌の運動能を亢進するPoster presentation
- 第37回分子病理学研究会, Jul. 2018, Japanese, 分子病理学研究会, 佐賀市, Domestic conference免疫染色画像ソフトウエアを用いた食道扁平上皮癌組織免疫染色画像のマクロファージ形態計測Poster presentation
- 第27回日本がん転移学会学術集会, Jul. 2018, Japanese, 日本がん転移学会, 横浜市, Domestic conferenceGDF15はTGF-βRIIの活性化を介して食道扁平上皮癌の増殖能と運動・浸潤能を亢進させるPublic symposium
- 第107回日本病理学会総会, Jun. 2018, Japanese, 日本病理学会, 札幌市, Domestic conference微小環境における腫瘍関連マクロファージ由来のCXCL8はヒト食道扁平上皮癌の運動能および浸潤能を促進するPoster presentation
- 第107回日本病理学会総会・学術大会, Jun. 2018, Japanese, 札幌, Domestic conference微小環境における腫瘍関連マクロファージ由来のCXCL8はヒト食道扁平上皮癌の運動能および浸潤能を促進するPoster presentation
- 第107回日本病理学会総会, Jun. 2018, Japanese, 日本病理学会, 札幌市, Domestic conference頭頸部腺様嚢胞癌63例の臨床病理学的検討Poster presentation
- 第107回日本病理学会総会, Jun. 2018, Japanese, 日本病理学会, 札幌市, Domestic conference食道扁平上皮癌微小環境におけるFAP陽性癌関連線維芽細胞の役割Oral presentation
- 第107回日本病理学会総会・学術大会, Jun. 2018, Japanese, 札幌, Domestic conference食道扁平上皮癌微小環境におけるFAP陽性癌関連線維芽細胞の役割Oral presentation
- 第107回日本病理学会総会, Jun. 2018, Japanese, 日本病理学会, 札幌市, Domestic conference食道扁平上皮癌と腫瘍関連マクロファージとの相互作用はCCL2/CCR2経路の活性化を介して癌進展に関与するOral presentation
- 第107回日本病理学会総会・学術大会, Jun. 2018, Japanese, 札幌, Domestic conference食道扁平上皮癌と腫瘍関連マクロファージとの相互作用はCCL2/CCR2経路の活性化を介して癌進展に関与するPoster presentation
- 第107回日本病理学会総会・学術大会, Jun. 2018, Japanese, 札幌, Domestic conference腫瘍微小環境の病理学 がん細胞、腫瘍随伴マクロファージおよびがん関連線維芽細胞の相互作用による腫瘍促進的微小環境の形成[Invited]Nominated symposium
- 第107回日本病理学会総会, Jun. 2018, Japanese, 日本病理学会, 札幌市, Domestic conference腫瘍関連マクロファージ（TAM）との共培養により食道扁平上皮癌細胞で誘導されるANXA10の解析Poster presentation
- 第107回日本病理学会総会・学術大会, Jun. 2018, Japanese, 札幌, Domestic conference腫瘍関連マクロファージ(TAM)との共培養により食道扁平上皮癌細胞で誘導されるANXA10の解析Poster presentation
- 第107回日本病理学会総会, Jun. 2018, Japanese, 日本病理学会, 札幌市, Domestic conference口腔扁平上皮癌の発癌初期段階におけるマクロファージ浸潤の意義Poster presentation
- 第107回日本病理学会総会・学術大会, Jun. 2018, Japanese, 札幌, Domestic conference口腔扁平上皮癌の発癌初期段階におけるマクロファージ浸潤の意義Oral presentation
- 第107回日本病理学会総会, Jun. 2018, Japanese, 日本病理学会, 札幌市, Domestic conferenceマクロファージと食道扁平上皮細胞との相互作用によってCSF3/G-CSF経路が促進するPoster presentation
- 第107回日本病理学会総会・学術大会, Jun. 2018, Japanese, Domestic conferenceマクロファージと食道扁平上皮細胞との相互作用によってCSF3/G-CSF経路が促進するOral presentation
- 第107回日本病理学会総会, Jun. 2018, Japanese, 日本病理学会, 札幌市, Domestic conferenceがん細胞、腫瘍随伴マクロファージおよびがん関連線維芽細胞の相互作用による腫瘍促進的微小環境の形成[Invited]Nominated symposium
- 第107回日本病理学会総会, Jun. 2018, Japanese, 日本病理学会, 札幌市, Domestic conferenceGDF15はTGF-βRIIの活性化を介して食道扁平上皮癌細胞の増殖能と運動・浸潤能を亢進させるOral presentation
- 第107回日本病理学会総会・学術大会, Jun. 2018, Japanese, 札幌, Domestic conferenceGDF15はTGF-βRIIの活性化を介して食道扁平上皮癌細胞の増殖能と運動・浸潤能を亢進させるPoster presentation
- 第107回日本病理学会総会・学術大会, Apr. 2018, Japanese, 札幌, Domestic conference免疫染色画像解析ソフトウェアを用いた食道扁平上皮癌組織免疫染色画像のマクロファージ形態計測Poster presentation
- 第28回日本消化器癌発生学会総会, Nov. 2017, Japanese, 日本消化器癌発生学会, 熊本, Domestic conference食道扁平上皮癌微小環境におけるFAP陽性癌関連線維芽細胞の役割Poster presentation
- 第28回日本消化器癌発生学会総会, Nov. 2017, English, 日本消化器癌発生学会, 熊本, Domestic conferenceCXCL8 derived from TAMs promotes cell migration and invasion of human esophageal cancer cells[Invited]Invited oral presentation
- 第37回日本分子腫瘍マーカー研究会, Sep. 2017, Japanese, 日本分子腫瘍マーカー研究会, 横浜, Domestic conference食道扁平上皮癌微小環境におけるFAP陽性癌関連線維芽細胞の役割Oral presentation
- 第78回日本癌学会学術総会, Sep. 2017, Japanese, 日本癌学会, 横浜, Domestic conferenceRoles of Cyr61 in human esophageal squamous cell carcinoma microenvironmentPoster presentation
- 第78回日本癌学会学術総会, Sep. 2017, Japanese, 日本癌学会, 横浜, Domestic conferencePseudocolor IHC imaging cytometry of macrophages and localization analysis of signaling proteins in the ESCC tissuesPoster presentation
- 第78回日本癌学会学術総会, Sep. 2017, Japanese, 日本癌学会, 横浜, Domestic conferenceInteraction between esophageal squamous cell carcinoma and macrophage promotes cancer progression via CCL2/CCR2 axisOral presentation
- 第78回日本癌学会学術総会, Sep. 2017, Japanese, 日本癌学会, 横浜, Domestic conferenceRole of cancer-associated fibroblasts in the esophageal squamous cell carcinoma microenvironmentPoster presentation
- 第78回日本癌学会学術総会, Sep. 2017, Japanese, 日本癌学会, 横浜, Domestic conferenceAnalysis of genes induced by the co-culture of esophageal cancer cells with tumor- associated macrophagesPoster presentation
- 第78回日本癌学会学術総会, Sep. 2017, Japanese, 日本癌学会, 横浜, Domestic conferenceCXCL8 derived from TAMs promotes cell migration and invasion of human esophageal cancer cellsOral presentation
- 第78回日本癌学会学術総会, Sep. 2017, Japanese, 日本癌学会, 横浜, Domestic conferenceGDF15 promotes cell proliferation, migration and invasion of esophageal squamous cell carcinoma via TGF-beta RII activationPoster presentation
- 第26回日本がん転移学会学術集会・総会, Jul. 2017, Japanese, 日本がん転移学会, 大阪, Domestic conference食道扁平上皮癌微小環境におけるCyr61の役割Poster presentation
- 第14回日本病理学会カンファレンス, Jul. 2017, Japanese, 日本病理学会, 犬山, Domestic conference食道扁平上皮癌組織免疫染色像の擬似カラー化によるマクロファージ形態とシグナル伝達分子局在の可視化Poster presentation
- 第36回分子病理学研究会, Jul. 2017, Japanese, 分子病理学研究会, 宮崎, Domestic conference食道扁平上皮癌と腫瘍関連マクロファージとの相互作用は CCL2/CCR2 経路の活性化を介して癌進展に関与するPoster presentation
- 第72回日本消化器外科学会総会, Jul. 2017, English, 日本消化器外科学会, 金沢, Domestic conferenceThe role of cancer microenvironment in growth, invasion, and metastasis of cancer[Invited]Nominated symposium
- 第72回日本消化器外科学会総会, Jul. 2017, Japanese, 日本消化器外科学会, 金沢, Domestic conference癌微小環境における腫瘍関連マクロファージ由来のIL-8はヒト食道扁平上皮癌の運動能および浸潤能を促進するOral presentation
- 第36回分子病理学研究会, Jul. 2017, Japanese, 分子病理学研究会, 宮崎, Domestic conferenceGDF15 は TGF-βRII の活性化を介して食道扁平上皮癌細胞の増殖能・遊走能・浸潤能を亢進させるPoster presentation
- 第106回日本病理学会総会, Apr. 2017, Japanese, 日本病理学会, 東京, Domestic conferenceRole of cancer-associated fibroblasts in the esophageal squamous cell carcinoma microenvironmentPoster presentation
- 第106回日本病理学会総会, Apr. 2017, Japanese, 日本病理学会, 東京, Domestic conferenceRoles of Cyr61 in human esophageal squamous cell carcinoma microenvironmentPoster presentation
- 第106回日本病理学会総会, Apr. 2017, Japanese, 日本病理学会, 東京, Domestic conferencePseudocolor IHC imaging cytometry and visualization of signaling molecules in the ESCC tissuesPoster presentation
- 第106回日本病理学会総会, Apr. 2017, Japanese, 日本病理学会, 東京, Domestic conferenceInteraction between esophageal cancer and macrophage promotes cancer progression via CCL2/CCR2 axisPoster presentation
- 第106回日本病理学会総会, Apr. 2017, Japanese, 日本病理学会, 東京, Domestic conferenceAnalysis of genes induced in esophageal cancer cells co-cultured with tumor-associated macrophagesPoster presentation
- 第106回日本病理学会総会, Apr. 2017, Japanese, 日本病理学会, 東京, Domestic conferenceCCL3 derived from tumor-associated macrophage promotes cell migration of human esophageal cancerOral presentation
- 第106回日本病理学会総会, Apr. 2017, Japanese, 日本病理学会, 東京, Domestic conferenceIL-8 derived from TAMs promotes cell migration and invasion of human ESCC cellsOral presentation
- 第106回日本病理学会総会, Apr. 2017, Japanese, 日本病理学会, 東京, Domestic conferenceInteraction between macrophage and esophageal squamous epithelial cell enhances CSF3/G-CSF signalingOral presentation
- 第106回日本病理学会総会, Apr. 2017, Japanese, 日本病理学会, 東京, Domestic conferenceGDF15 promotes progression of esophageal squamous cell carcinoma via TGF-β RII activationPoster presentation
- 第89回日本胃癌学会総会, Mar. 2017, Japanese, Japanese Gastric Cancer Association, 広島, Domestic conference直接接触相互作用によるスキルス胃癌細胞の浸潤と間質線維芽細胞の増殖促進Poster presentation
- 第89回日本胃癌学会総会, Mar. 2017, Japanese, 一般社団法人 日本胃癌学会, 広島, Domestic conferenceThe cancer-stromal interaction in scirrhous-type gastric carcinoma（直接接触相互作用によるスキルス胃癌細胞の浸潤と間質線維芽細胞の増殖促進）Poster presentation
- 第62回日本病理学会秋期特別総会, Nov. 2016, Japanese, Japanese Society of Pathology, 金沢, Domestic conferenceAnalysis of genes induced by the co-culture of esophageal cancer cells with tumor associated macrophagesPoster presentation
- 第75回日本癌学会学術総会, Oct. 2016, English, Japanese Cancer Association, 横浜, Domestic conference食道扁平上皮癌組織でM2マクロファージは非癌部より伸長し、in vitro培養マクロファージ画像解析と合致するOral presentation
- 第75回日本癌学会学術総会, Oct. 2016, Japanese, Japanese Cancer Association, 横浜, Domestic conference腫瘍関連マクロファージと食道扁平上皮癌から分泌されるCCL2は食道扁平上皮癌細胞の運動能を亢進させるPoster presentation
- 第75回日本癌学会学術総会, Oct. 2016, Japanese, Japanese Cancer Association, 横浜, Domestic conference腫瘍関連マクロファージとの共培養により食道扁平上皮癌細胞に誘導される遺伝子の解析Poster presentation
- 第75回日本癌学会学術総会, Oct. 2016, Japanese, Japanese Cancer Association, 横浜, Domestic conference腫瘍関連マクロファージから分泌されるCCL3はヒト食道扁平上皮癌細胞の運動能を亢進させるPoster presentation
- 第75回日本癌学会学術総会, Oct. 2016, Japanese, Japanese Cancer Association, 横浜, Domestic conference癌微小環境における腫瘍関連マクロファージ由来のIL-8はヒト食道扁平上皮癌の運動能および浸潤能を促進するPoster presentation
- 第36回日本分子腫瘍マーカー研究会, Oct. 2016, Japanese, Japan Society for Molecular Tumor Marker Research, 横浜, Domestic conference癌微小環境における腫瘍関連マクロファージ由来のIL-8はヒト食道扁平上皮癌の運動能および浸潤能を促進するOral presentation
- 第75回日本癌学会学術総会, Oct. 2016, Japanese, Japanese Cancer Association, 横浜, Domestic conferenceヒト食道扁平上皮癌の発癌初期段階におけるマクロファージの機能解析Poster presentation
- 第75回日本癌学会学術総会, Oct. 2016, Japanese, Japanese Cancer Association, 横浜, Domestic conferenceヒト食道扁平上皮癌における腫瘍関連マクロファージの生存能および遊走能に対するNCAMの役割Poster presentation
- 第75回日本癌学会学術総会, Oct. 2016, Japanese, 日本癌学会, 横浜, Domestic conferenceRoles of macrophages in early squamous cell carcinogenesis of the esophagus(ヒト食道扁平上皮癌の発癌初期段階におけるマクロファージの機能解析)Poster presentation
- 第75回日本癌学会学術総会, Oct. 2016, Japanese, 日本癌学会, 横浜, Domestic conferenceRole of NCAM in cell survival and migration of TAMs in human esophageal squamous cell carcinoma(ヒト食道扁平上皮癌における腫瘍関連マクロファージの生存能および遊走能に対する NCAM の役割)Poster presentation
- 第75回日本癌学会学術総会, Oct. 2016, English, 日本癌学会, 横浜, Domestic conferenceM2-activated Mφs elongate in the ESCC tissues, consistent withthe in vitro cell image analyses（食道扁平上皮癌組織で M2 マクロファージは非癌部より伸長し、in vitro 培養マクロファージ画像解析と合致する)Oral presentation
- 第75回日本癌学会学術総会, Oct. 2016, Japanese, 日本癌学会, 横浜, Domestic conferenceIL-8 derived from TAMs promotes cell migration and invasion of human Esophageal cancer cells（癌微小環境における腫瘍関連マクロファージ由来の IL-8 はヒト食道扁平上皮癌の運動能および浸潤能を促進する）Poster presentation
- 第75回日本癌学会学術総会, Oct. 2016, Japanese, 日本癌学会, 横浜, Domestic conferenceCCL3 derived from tumor-associated macrophage promotes cell migration of human esophageal squamous cell carcinoma(腫瘍関連マクロファージから分泌される CCL3 はヒト食道扁平上皮癌細胞の運動能を亢進させる)Poster presentation
- 第75回日本癌学会学術総会, Oct. 2016, Japanese, 日本癌学会, 横浜, Domestic conferenceCCL2 derived from both tumor-associated macrophage and esophageal cancer promotes cell migration of cancer cell(腫瘍関連マクロファージと食道扁平上皮癌から分泌される CCL2 は食道扁平上皮癌細胞の運動能を亢進させる)Poster presentation
- 第27回日本消化器癌発生学会総会, Sep. 2016, Japanese, 日本消化器癌発生学会, 鹿児島, Domestic conference癌微小環境における腫瘍関連マクロファージ由来のIL-8はヒト食道扁平上皮癌の運動能および浸潤能を促進するOral presentation
- 第35回分子病理学研究会, Jul. 2016, Japanese, 分子病理学研究会, 横浜, Domestic conference食道扁平上皮癌組織でM2マクロファージは非癌部より伸長し、in vitro培養マクロファージ画像解析と合致するPoster presentation
- 第13回日本病理学会カンファレンス, Jul. 2016, Japanese, Japanese Society of Pathology, 神戸, Domestic conferenceマクロファージによるp38MAPキナーゼおよびIL-6の活性化は食道癌の発癌初期段階を促進するPoster presentation
- 第105回日本病理学会総会, May 2016, Japanese, Japanese Society of Pathology, 仙台, Domestic conference食道扁平上皮癌組織でM2マクロファージは非癌部より伸長し、in vitro培養マクロファージ画像解析と合致するOral presentation
- 第105回日本病理学会総会, May 2016, Japanese, Japanese Society of Pathology, 仙台, Domestic conference腫瘍関連マクロファージによるヒト食道扁平上皮癌進展機構の解明Poster presentation
- 第105回日本病理学会総会, May 2016, Japanese, Japanese Society of Pathology, 仙台, Domestic conference腫瘍関連マクロファージから分泌されるCCL3はヒト食道扁平上皮癌の運動能を亢進させるPoster presentation
- 第105回日本病理学会総会, May 2016, Japanese, Japanese Society of Pathology, 仙台, Domestic conference癌微小環境における腫瘍関連マクロファージ由来のIL-8はヒト食道扁平上皮癌の運動能および浸潤能を促進するPoster presentation
- 第105回日本病理学会総会, May 2016, Japanese, Japanese Society of Pathology, 仙台, Domestic conferenceヒト食道扁平上皮癌微小環境におけるFGF-2-NCAM/FGFR1相互作用の役割Oral presentation
- 第105回日本病理学会総会, May 2016, Japanese, Japanese Society of Pathology, 仙台, Domestic conferenceヒト食道扁平上皮癌の発癌初期段階におけるマクロファージの機能解析Poster presentation
- AACR Annual Meeting 2016, Apr. 2016The roles of FGF2-NCAM/FGFR1 interplay in esophageal squamous cell carcinomas and its microenvironment including tumor-associated macrophages
- AACR Annual Meeting 2016, Apr. 2016, English, American Association for Cancer Research, New Orleans, USA, International conferenceThe roles of FGF-2-NCAM/FGFR1 interplay in esophageal squamous cell carcinomas and its microenvironment including tumor-associated macrophages.Poster presentation
- Tenth AACR-JCA Joint Conference, Feb. 2016Infiltrating macrophages may promote early esophageal carcinogenesis via p38 MAP kinase and IL-6 signaling
- 第26回日本消化器癌発生学会総会, Nov. 2015, Japanese, 日本消化器癌発生学会, 米子, Domestic conferenceNCAMとFGFRの相互作用はヒト食道扁平上皮癌における腫瘍関連マクロファージの生存能および遊走能に関与するOral presentation
- 第26回日本消化器癌発生学会, Nov. 2015, Japanese, The Japanese Society for Gastroenterological Carcinogenesis, 米子, Domestic conferenceNCAMとFGFRの相互作用はヒト食道癌における腫瘍関連マクロファージの生存能および遊走能に関与するOral presentation
- 第74回日本癌学会総会学術集会, Oct. 2015, Japanese, The Japanese Cancer Association, 名古屋, Domestic conference食道扁平上皮癌微小環境におけるCyr61の役割Poster presentation
- 第74回日本癌学会総会学術集会, Oct. 2015, Japanese, The Japanese Cancer Association, 名古屋, Domestic conference腫瘍関連マクロファージから分泌されるCCL3はAktとERKの経路を介して食道扁平上皮癌の運動能を亢進させるPoster presentation
- 第74回日本癌学会総会学術集会, Oct. 2015, Japanese, The Japanese Cancer Association, 名古屋, Domestic conference腫瘍関連マクロファージおよび癌細胞が分泌するGDF15は食道扁平上皮癌の腫瘍増殖、進展に関与するPoster presentation
- 第74回日本癌学会総会学術集会, Oct. 2015, Japanese, The Japanese Cancer Association, 名古屋, Domestic conferenceマクロファージによるp38MAPキナーゼおよびIL-6の活性化は食道癌の発癌初期段階を促進するOral presentation
- 第74回日本癌学会総会学術集会, Oct. 2015, Japanese, The Japanese Cancer Association, 名古屋, Domestic conferenceヒト単球由来マクロファージのTAM様形態変化は核面積、細胞質面積、細胞質縦横比の増加と核胞体比の減少に反映されるPoster presentation
- 第35回日本分子腫瘍マーカー研究会, Oct. 2015, Japanese, Japan Society for Molecular Tumor Marker Research, 名古屋, Domestic conferenceヒト単球由来マクロファージのTAM様形態変化は核および細胞質の面積、長径、短径、細胞質縦横比の増加と核胞体比の減少に反映されるOral presentation
- 第74回日本癌学会学術総会, Oct. 2015, Japanese, 名古屋, Domestic conferenceRole of Cyr61 in esophageal squamouscell carcinoma microenvironmentPoster presentation
- 第74回日本癌学会総会学術集会, Oct. 2015, Japanese, The Japanese Cancer Association, 名古屋, Domestic conferenceNCAMはヒト食道扁平上皮癌における腫瘍関連マクロファージの生存能および遊走能に関与するOral presentation
- European Cancer Congress, Sep. 2015Contribution of cancer-associated fibroblasts and M2-polarized macrophages to neuroblastoma development
- 第34回分子病理学研究会 神戸シンポジウム, Jul. 2015, Japanese, 分子病理学研究会, 神戸, Domestic conferenceマクロファージによるp38MAPキナーゼおよびIL-6の活性化は食道癌の発癌初期段階を促進するPoster presentation
- 第12回日本病理学会カンファレンス, Jul. 2015, Japanese, The Japanese Sciety of Pathology, 神戸, Domestic conferenceNCAMはヒト食道癌における腫瘍関連マクロファージの生存能および遊走能に関与するPoster presentation
- 第104回日本病理学会総会・学術大会, May 2015, Japanese, Domestic conference食道扁平上皮癌においてCyr61はマクロファージのCD204発現誘導および遊走能を亢進するPoster presentation
- 第104回日本病理学会総会, May 2015, Japanese, The Japanese Sciety of Pathology, 名古屋, Domestic conference食道上皮内マクロファージ密度と上皮増殖性病変分布の相関Poster presentation
- 第104回日本病理学会総会, May 2015, Japanese, The Japanese Sciety of Pathology, 名古屋, Domestic conference腫瘍関連マクロファージから分泌されるIL-24によるヒト食道扁平上皮癌の進展機構の解明Poster presentation
- 第104回日本病理学会総会, May 2015, Japanese, The Japanese Sciety of Pathology, 名古屋, Domestic conference癌微小環境中のGDF15は食道扁平上皮癌の増殖・浸潤を促進するPoster presentation
- 第104回日本病理学会総会, May 2015, Japanese, The Japanese Sciety of Pathology, 名古屋, Domestic conferenceマクロファージによるp38 MAPキナーゼの活性化は食道癌の発癌初期段階を促進するOral presentation
- 第104回日本病理学会総会, May 2015, Japanese, The Japanese Sciety of Pathology, 名古屋, Domestic conferenceヒト単球由来マクロファージのTAM様形態変化は細胞質縦横比のみならず核面積と核胞体面積比にも反映されるPoster presentation
- 第104回日本病理学会総会, May 2015, Japanese, The Japanese Sciety of Pathology, 名古屋, Domestic conferenceNCAMはヒト食道癌における腫瘍関連マクロファージの生存能および浸潤能に関与するPoster presentation
- 第104回日本病理学会総会, Apr. 2015, Japanese, The Japanese Sciety of Pathology, 名古屋, Domestic conference神経芽腫の進展における腫瘍関連炎症細胞と腫瘍関連間質細胞の相互作用の解明Oral presentation
- 第104回日本病理学会総会, Apr. 2015, Japanese, The Japanese Sciety of Pathology, 名古屋, Domestic conference食道扁平上皮癌微小環境においてCyr61はマクロファージのCD204発現誘導および遊走能を亢進するPoster presentation
- 第104回日本病理学会総会, Apr. 2015, Japanese, The Japanese Sciety of Pathology, 名古屋, Domestic conference食道扁平上皮癌の増殖、進展と腫瘍組織内CD204陽性マクロファージの関連Poster presentation
- 第104回日本病理学会総会, Apr. 2015, Japanese, The Japanese Sciety of Pathology, 名古屋, Domestic conferenceマクロファージによるCCL3-CCR1経路の活性化はヒト食道扁平上皮癌の運動能を亢進させるPoster presentation
- 第25回日本消化器癌発生学会総会, Nov. 2014, Japanese, 日本消化器癌発生学会, 福岡, Domestic conference腫瘍関連マクロファージが分泌するGDF15は食道扁平上皮癌の腫瘍増殖、進展に関与するOral presentation
- The 73rd Annual Meeting of the Japanese Cancer Association, Sep. 2014, Japanese, Japanese Cancer Association, 横浜, Domestic conferenceRole of Cyr61 in esophageal squamous cell carcinoma microenvironmentOral presentation
- The 73rd Annual Meeting of the Japanese Cancer Association, Sep. 2014, Japanese, Japanese Cancer Association, 横浜, Domestic conferenceClinicopathological significance of GDF15 in the microenvironment of human esophageal squamous cell carcinomaPoster presentation
- The 73rd Annual Meeting of the Japanese Cancer Association, Sep. 2014, Japanese, Japanese Cancer Association, 横浜, Domestic conferenceTumor associated macrophage-derived GDF15 induces phosphorylation of Akt and Erk in esophageal squamous cell carcinomaPoster presentation
- The 73rd Annual Meeting of the Japanese Cancer Association, Sep. 2014, Japanese, Japanese Cancer Association, 横浜, Domestic conferenceImage analysis of morphological changes and M2 marker expression of human peripheral blood monocytes derived macrophagesPoster presentation
- The 73rd Annual Meeting of the Japanese Cancer Association, Sep. 2014, Japanese, Japanese Cancer Association, 横浜, Domestic conferenceInfiltrating macrophages may promote early esophageal carcinogenesis via p38 MAP kinase cascadePoster presentation
- 第34回日本分子腫瘍マーカー研究会, Sep. 2014, Japanese, 日本分子腫瘍マーカー研究会, 横浜, Domestic conferenceマクロファージによるp38 MAP kinaseカスケードの活性化は食道癌の発癌初期段階を促進するOral presentation
- The 73rd Annual Meeting of the Japanese Cancer Association, Sep. 2014, Japanese, Japanese Cancer Association, 横浜, Domestic conferenceNCAM is contributed to cell proliferation and invasion of tumor associated macrophage in human esophageal cancerPoster presentation
- 第11回日本病理学会カンファレンス, Aug. 2014, Japanese, 日本病理学会, 神戸, Domestic conference蛍光画像ソフトウエアによるヒト単球由来マクロファージのTAM様形態変化とM2マーカータンパク発現の定量評価Poster presentation
- 第33回分子病理学研究会, Jul. 2014, Japanese, 分子病理学研究会, 宮城蔵王, Domestic conference腫瘍関連マクロファージから分泌されるGDF15はヒト食道扁平上皮癌細胞株の生存に寄与するPoster presentation
- 第33回分子病理学研究会, Jul. 2014, Japanese, 分子病理学研究会, 宮城蔵王, Domestic conferenceヒト食道扁平上皮癌における腫瘍関連マクロファージで高発現する接着分子NCAMの機能解析Poster presentation
- 第103回日本病理学会総会・学術大会, Apr. 2014, Japanese, 広島, Domestic conference食道扁平上皮癌微小環境においてCyr61はマクロファージのCD204発現誘導および遊走能を亢進するOral presentation
- 第103回日本病理学会総会, Apr. 2014, Japanese, 日本病理学会, 広島, Domestic conference食道扁平上皮癌微小環境においてCyr61はマクロファージのCD204発現誘導および遊走能を亢進するOral presentation
- 第103回日本病理学会総会, Apr. 2014, Japanese, 日本病理学会, 広島, Domestic conference食道扁平上皮癌に浸潤する腫瘍組織内CD204陽性マクロファージは腫瘍増殖、進展に関与するPoster presentation
- 第103回日本病理学会総会, Apr. 2014, Japanese, 日本病理学会総会, 広島, Domestic conference腫瘍関連マクロファージで高発現する接着分子や細胞外基質の機能解析Poster presentation
- 第103回日本病理学会総会, Apr. 2014, Japanese, 日本病理学会, 広島, Domestic conference腫瘍関連マクロファージから分泌されるケモカインによるヒト食道扁平上皮癌の進展機構の解明Poster presentation
- 第103回日本病理学会総会, Apr. 2014, Japanese, 日本病理学会, 広島, Domestic conference腫瘍関連マクロファージから分泌されるGDF15はヒト食道扁平上皮癌細胞株のAKTとERK1/2の経路を活性化させるPoster presentation
- 第103回日本病理学会総会, Apr. 2014, Japanese, 日本病理学会, 広島, Domestic conference蛍光画像解析ソフトによるヒト単球由来マクロファージのTAM様変化とM2マーカータンパク発現の定量評価Poster presentation
- 第103回日本病理学会総会, Apr. 2014, Japanese, 日本病理学会, 広島, Domestic conferenceヒト食道扁平上皮癌の発癌初期段階におけるマクロファージの機能解析Poster presentation
- The 4th JCA-AACR Special Joint Conference, Dec. 20134. Direct cancer-stromal interaction increases fibroblast proliferation and enhances invasive properties of scirrhous-type gastric carcinoma cells
- The 4th JCA-AACR Special Joint Conference:The Latest Advances in Gastric Cancer Research:, Dec. 2013, English, JCA-AACR, Urayasu, gastric cancer, fibroblast, International conferenceDirect cancer-stromal interaction increases fibroblast proliferation and enhances invasive properties of scirrhous-type gastric carcinoma cellsPoster presentation
- The Latest Advances in Gastric Cancer Research, Nov. 2013, Japanese, 東京, Domestic conferenceDirect cancer-stromal interaction increases fibroblast proliferation and enhances invasive properties of scirrhous-type gastric carcinoma cellsOral presentation
- 第33回日本分子腫瘍マーカー研究会, Oct. 2013, Japanese, 日本分子腫瘍マーカー研究会, 横浜, Domestic conference食道扁平上皮癌の増殖、進展と腫瘍組織内CD204陽性マクロファージの関連Oral presentation
- 第72回日本癌学会総会, Oct. 2013, Japanese, 日本癌学会, 横浜, Domestic conference食道上皮内マクロファージ密度と上皮増殖性病変分布の相関Poster presentation
- The 72nd Annual Meeting of the Japanese Cancer Association, Oct. 2013, Japanese, JAPANESE CANCER ASSOCIATION, 横浜, Domestic conference食道癌におけるCD204陽性腫瘍関連マクロファージの臨床病理学的検討Poster presentation
- 第72回日本癌学会総会, Oct. 2013, Japanese, 日本癌学会, 横浜, Domestic conferenceヒト末梢血単球由来マクロファージは食道癌細胞株培養上清により腫瘍関連マクロファージとしての形質を獲得するPoster presentation
- 第72回日本癌学会総会, Oct. 2013, Japanese, 日本癌学会, 横浜, Domestic conferenceIn vitroにおいてマクロファージは食道癌細胞によりM2型へと分化し、IL-11の発現を上昇させるPoster presentation
- The 72nd Annual Meeting of the Japanese Cancer Association, Oct. 2013, English, Annual Meeting of the Japanese Cancer Association, 横浜, International conferenceIn vitro interaction with esophageal cancer cells induce M2 differentiation and IL-11 upregulation in macrophages.．Oral presentation
- 第72回日本癌学会学術総会, Oct. 2013, Japanese, 横浜, Domestic conferenceIn vitro interaction with esophageal cancer cells induce M2 differentiation and IL-11 upregulation in macrophagesPoster presentation
- 第10回日本病理学会カンファレンス2013六甲山, Aug. 2013, Japanese, 日本病理学会, 神戸, Domestic conference食道扁平上皮癌の増殖、進展と腫瘍組織内CD204陽性マクロファージの関連Poster presentation
- 第10回日本病理学会カンファレンス2013六甲山, Aug. 2013, Japanese, 日本病理学会, 神戸, Domestic conferenceヒト単球系細胞株THP-1を用いた食道癌の増殖促進における腫瘍組織内マクロファージのin vitro解析Poster presentation
- 第10回日本病理学会カンファレンス, Aug. 2013, Japanese, Domestic conferenceヒト単球系細胞株THP-1を用いた食道癌の増殖進展における腫瘍組織内マクロファージのin vitro解析Poster presentation
- 第32回分子病理研究会吉野シンポジウム, Jul. 2013, Japanese, 奈良, Domestic conference食道扁平上皮癌におけるCD204陽性マクロファージの役割Poster presentation
- 第32回分子病理学研究会吉野シンポジウム, Jul. 2013, Japanese, 分子病理学研究会, 奈良県吉野町, Domestic conference食道扁平上皮癌におけるCD204陽性マクロファージの役割Poster presentation
- 第102回日本病理学会総会, Jun. 2013, Japanese, 日本病理学会, 札幌, Domestic conference食道上皮内マクロファージ密度と上皮増殖性病変分布の相関Poster presentation
- 第102回日本病理学会総会, Jun. 2013, Japanese, 日本病理学会, 札幌, Domestic conferenceヒト末梢血単球由来マクロファージは食道癌細胞株培養上清により腫瘍関連マクロファージの形質を獲得するPoster presentation
- 第102回日本病理学会総会, Jun. 2013, Japanese, 日本病理学会, 札幌, Domestic conferenceヒト単球系細胞株THP－1を用いた食道癌の増殖進展における腫瘍組織内マクロファージのin vitro解析Oral presentation
- 第102回日本病理学会総会・学術大会, Jun. 2013, Japanese, 札幌, Domestic conferenceヒト単球系細胞株THP-1を用いた食道癌の増殖進展における腫瘍組織内マクロファージのin vitro解析Poster presentation
- 第102回日本病理学会総会, Jun. 2013, Japanese, 日本病理学会, 札幌, Domestic conferencePTTM (pulmonary tumor thrombotic microangiopathy) の2剖検例Poster presentation
- 第102回日本病理学会総会, Jun. 2013, Japanese, 日本病理学会, 札幌, Domestic conferenceALK融合遺伝子陽性肺癌の検出を目的としたFISH検査の施設間差についてOral presentation
- 第101回日本病理学会総会, Apr. 2012, Japanese, The Japanese Society of Pathology, 東京, Domestic conferenceALK肺癌の術前診断の検討 形態、免疫染色、FISHPoster presentation
- Fifteenth International Symposium of the Hiroshima Cancer Seminar, Oct. 2005Expression of PRL-3 contributes to cell motility and proliferation.
- Fifteenth International Symposium of the Hiroshima Cancer Seminar, Oct. 2005【優秀ポスター演題賞受賞】Localization of the PP2A B56ɤ regulatory subunit at the golgi complex -possible role in vesicle transport and migration-
- 第14回日本がん転移学会総会, Jun. 2005【受賞講演】脱リン酸化酵素変異による癌進展機構の解析-遺伝子不安定性の増大と小胞輸送の加速化-[Invited]Invited oral presentation
- 4th International Conference on Protein Phosphatases, Nov. 2000Possible role of the PP2A B56ɤ 1 regulatory subunit for post-Golgi membrane trafficking of adhesion molecules
- American Society for Investigative Pathology
- International Academy of Pathology
- 日本消化器癌発生学会
- 日本分子腫瘍マーカー研究会
- 日本がん転移学会
- 日本臨床細胞学会
- 日本癌学会
- 日本病理学会
- 日本学術振興会, 科学研究費助成事業, 基盤研究(C), 神戸大学, Apr. 2025 - Mar. 2028新規治療標的分子の探索を目指した食道扁平上皮癌における癌間質相互作用の解析
- 日本学術振興会, 科学研究費助成事業 基盤研究(C), 基盤研究(C), 神戸大学, Apr. 2022 - Mar. 2025, Principal investigator癌細胞と間質細胞との直接接触による細胞間相互作用を介した食道癌の進展機構の解析
- 公益財団法人 武田科学振興財団, 医学系研究助成（がん領域）, 医学系研究助成（がん領域）, Aug. 2021癌細胞と間質細胞との３次元共培養による食道扁平上皮癌微小環境の解析
- 学術研究助成基金助成金／基盤研究(C), Apr. 2018 - Mar. 2021, Principal investigatorCompetitive research funding
- 消化器癌発生学会, 消化器癌発生学会・理事長直轄プロジェクト 特別研究推進, 腫瘍-間質相互作用を標的とした癌進展メカニズムの解明, 2018 - 2019
- 学術研究助成基金助成金／若手研究(B), Apr. 2016 - Mar. 2018, Principal investigatorCompetitive research funding
- 学術研究助成基金助成金／若手研究(B), Apr. 2014 - Mar. 2016, Principal investigatorCompetitive research funding
- 一般社団法人神緑会, 一般社団法人神緑会研究助成金, Jun. 2015事業名『第35回日本分子腫瘍マーカー研究会・特別講演およびシンポジウム』